1
40
18
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1038/onc.2015.83" target="_blank" rel="noreferrer noopener">http://doi.org/10.1038/onc.2015.83</a>
Pages
314–322
Issue
3
Volume
35
Dublin Core
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Title
A name given to the resource
Activation of mechanosensitive ion channel TRPV4 normalizes tumor vasculature and improves cancer therapy.
Publisher
An entity responsible for making the resource available
Oncogene
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-01
Subject
The topic of the resource
Animals; Calcium Signaling/genetics; Carcinoma; Cell Line; Cell Proliferation/drug effects; Cisplatin/administration & dosage; Endothelium; Gene Expression Regulation; Humans; Leucine/administration & dosage/analogs & derivatives; Lewis Lung/drug therapy/*genetics/pathology; Mice; Neoplastic/drug effects; Neovascularization; Pathologic/drug therapy/*genetics/pathology; Sulfonamides/administration & dosage; TRPV Cation Channels/agonists/biosynthesis/*genetics; Tumor; Vascular Endothelial Growth Factor A/genetics; Vascular/drug effects/*pathology
Creator
An entity primarily responsible for making the resource
Adapala R K; Thoppil R J; Ghosh K; Cappelli H C; Dudley A C; Paruchuri S; Keshamouni V; Klagsbrun M; Meszaros J G; Chilian W M; Ingber D E; Thodeti C K
Description
An account of the resource
Tumor vessels are characterized by abnormal morphology and hyperpermeability that together cause inefficient delivery of chemotherapeutic agents. Although vascular endothelial growth factor has been established as a critical regulator of tumor angiogenesis, the role of mechanical signaling in the regulation of tumor vasculature or tumor endothelial cell (TEC) function is not known. Here we show that the mechanosensitive ion channel transient receptor potential vanilloid 4 (TRPV4) regulates tumor angiogenesis and tumor vessel maturation via modulation of TEC mechanosensitivity. We found that TECs exhibit reduced TRPV4 expression and function, which is correlated with aberrant mechanosensitivity towards extracellular matrix stiffness, increased migration and abnormal angiogenesis by TEC. Further, syngeneic tumor experiments revealed that the absence of TRPV4 induced increased vascular density, vessel diameter and reduced pericyte coverage resulting in enhanced tumor growth in TRPV4 knockout mice. Importantly, overexpression or pharmacological activation of TRPV4 restored aberrant TEC mechanosensitivity, migration and normalized abnormal angiogenesis in vitro by modulating Rho activity. Finally, a small molecule activator of TRPV4, GSK1016790A, in combination with anticancer drug cisplatin, significantly reduced tumor growth in wild-type mice by inducing vessel maturation. Our findings demonstrate TRPV4 channels to be critical regulators of tumor angiogenesis and represent a novel target for anti-angiogenic and vascular normalization therapies.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1038/onc.2015.83" target="_blank" rel="noreferrer noopener">10.1038/onc.2015.83</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2016
Adapala R K
Animals
Calcium Signaling/genetics
Cappelli H C
Carcinoma
Cell Line
Cell Proliferation/drug effects
Chilian W M
Cisplatin/administration & dosage
Department of Integrative Medical Sciences
Dudley A C
Endothelium
Gene Expression Regulation
Ghosh K
Humans
Ingber D E
Keshamouni V
Klagsbrun M
Leucine/administration & dosage/analogs & derivatives
Lewis Lung/drug therapy/*genetics/pathology
Meszaros J G
Mice
NEOMED College of Medicine
Neoplastic/drug effects
Neovascularization
Oncogene
Paruchuri S
Pathologic/drug therapy/*genetics/pathology
Sulfonamides/administration & dosage
Thodeti C K
Thoppil R J
TRPV Cation Channels/agonists/biosynthesis/*genetics
Tumor
Vascular Endothelial Growth Factor A/genetics
Vascular/drug effects/*pathology
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1007/s00395-016-0539-4" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s00395-016-0539-4</a>
Pages
21–21
Issue
2
Volume
111
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Differential regulation of TRPV1 channels by H2O2: implications for diabetic microvascular dysfunction.
Publisher
An entity responsible for making the resource available
Basic research in cardiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-03
Subject
The topic of the resource
*Coronary Circulation; *Microcirculation; Animals; Capsaicin; Coronary blood flow; Diabetic Angiopathies/*metabolism; HEK293 Cells; Humans; Hydrogen peroxide; Hydrogen Peroxide/*metabolism; Inbred C57BL; Knockout; Male; Mice; Reactive oxygen species; TRPV Cation Channels/*metabolism; TRPV1
Creator
An entity primarily responsible for making the resource
DelloStritto Daniel J; Connell Patrick J; Dick Gregory M; Fancher Ibra S; Klarich Brittany; Fahmy Joseph N; Kang Patrick T; Chen Yeong-Renn; Damron Derek S; Thodeti Charles K; Bratz Ian N
Description
An account of the resource
We demonstrated previously that TRPV1-dependent coupling of coronary blood flow (CBF) to metabolism is disrupted in diabetes. A critical amount of H2O2 contributes to CBF regulation; however, excessive H2O2 impairs responses. We sought to determine the extent to which differential regulation of TRPV1 by H2O2 modulates CBF and vascular reactivity in diabetes. We used contrast echocardiography to study TRPV1 knockout (V1KO), db/db diabetic, and wild type C57BKS/J (WT) mice. H2O2 dose-dependently increased CBF in WT mice, a response blocked by the TRPV1 antagonist SB366791. H2O2-induced vasodilation was significantly inhibited in db/db and V1KO mice. H2O2 caused robust
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1007/s00395-016-0539-4" target="_blank" rel="noreferrer noopener">10.1007/s00395-016-0539-4</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Coronary Circulation
*Microcirculation
2016
Animals
Basic research in cardiology
Bratz Ian N
Capsaicin
Chen Yeong-Renn
Connell Patrick J
Coronary blood flow
Damron Derek S
DelloStritto Daniel J
Department of Integrative Medical Sciences
Diabetic Angiopathies/*metabolism
Dick Gregory M
Fahmy Joseph N
Fancher Ibra S
HEK293 Cells
Humans
Hydrogen peroxide
Hydrogen Peroxide/*metabolism
Inbred C57BL
Kang Patrick T
Klarich Brittany
Knockout
Male
Mice
NEOMED College of Medicine
reactive oxygen species
Thodeti Charles K
TRPV Cation Channels/*metabolism
TRPV1
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.freeradbiomed.2016.09.021" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.freeradbiomed.2016.09.021</a>
Pages
10–19
Volume
101
Dublin Core
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Title
A name given to the resource
4-Hydroxynonenal dependent alteration of TRPV1-mediated coronary microvascular signaling.
Publisher
An entity responsible for making the resource available
Free radical biology & medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-12
Subject
The topic of the resource
*4-Hydroxynonenal; *Coronary regulation; *Lipid peroxidation; *Post-translational modification; *Protein Processing; *Reactive oxygen species; *Signal Transduction; *TRPV1; Action Potentials/drug effects; Aldehydes/antagonists & inhibitors/metabolism/*pharmacology; Animal; Animals; Blood Flow Velocity; Calcium Signaling/drug effects; Capsaicin/*pharmacology; Cardiovascular Agents/*pharmacology; Coronary Circulation/drug effects; Coronary Vessels/metabolism/physiopathology; Cysteine/genetics/metabolism; Diabetes Mellitus/drug therapy/*metabolism/physiopathology; Disease Models; Femoral Artery/metabolism/physiopathology; HEK293 Cells; Humans; Inbred C57BL; Lipid Peroxidation; Male; Mice; Patch-Clamp Techniques; Post-Translational; TRPV Cation Channels/genetics/*metabolism; Vasodilation/drug effects
Creator
An entity primarily responsible for making the resource
DelloStritto Daniel J; Sinharoy Pritam; Connell Patrick J; Fahmy Joseph N; Cappelli Holly C; Thodeti Charles K; Geldenhuys Werner J; Damron Derek S; Bratz Ian N
Description
An account of the resource
We demonstrated previously that TRPV1-dependent regulation of coronary blood flow (CBF) is disrupted in diabetes. Further, we have shown that endothelial TRPV1 is differentially regulated, ultimately leading to the inactivation of TRPV1, when exposed to a prolonged pathophysiological oxidative environment. This environment has been shown to increase lipid peroxidation byproducts including
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.freeradbiomed.2016.09.021" target="_blank" rel="noreferrer noopener">10.1016/j.freeradbiomed.2016.09.021</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*4-Hydroxynonenal
*Coronary regulation
*Lipid peroxidation
*Post-translational modification
*Protein Processing
*Reactive oxygen species
*Signal Transduction
*TRPV1
2016
Action Potentials/drug effects
Aldehydes/antagonists & inhibitors/metabolism/*pharmacology
Animal
Animals
Blood Flow Velocity
Bratz Ian N
Calcium Signaling/drug effects
Cappelli Holly C
Capsaicin/*pharmacology
Cardiovascular Agents/*pharmacology
Connell Patrick J
Coronary Circulation/drug effects
Coronary Vessels/metabolism/physiopathology
Cysteine/genetics/metabolism
Damron Derek S
DelloStritto Daniel J
Department of Integrative Medical Sciences
Diabetes Mellitus/drug therapy/*metabolism/physiopathology
Disease Models
Fahmy Joseph N
Femoral Artery/metabolism/physiopathology
Free radical biology & medicine
Geldenhuys Werner J
HEK293 Cells
Humans
Inbred C57BL
Lipid Peroxidation
Male
Mice
NEOMED College of Medicine
Patch-Clamp Techniques
Post-Translational
Sinharoy Pritam
Thodeti Charles K
TRPV Cation Channels/genetics/*metabolism
Vasodilation/drug effects
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1194/jlr.M064709" target="_blank" rel="noreferrer noopener">http://doi.org/10.1194/jlr.M064709</a>
Pages
1144–1154
Issue
7
Volume
57
Dublin Core
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Title
A name given to the resource
Cholesterol 7alpha-hydroxylase-deficient mice are protected from high-fat/high-cholesterol diet-induced metabolic disorders.
Publisher
An entity responsible for making the resource available
Journal of lipid research
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-07
Subject
The topic of the resource
*bile acids and salt/metabolism; *cholesterol/diet; *lipids; *liver; Animal; Animals; Bile Acids and Salts/genetics/metabolism; Cholesterol 7-alpha-Hydroxylase/*genetics/metabolism; Cholesterol/*metabolism; Diet; Disease Models; Exhalation/genetics; Glucose/metabolism; High-Fat; Homeostasis; Humans; Lipid Metabolism/genetics; Liver/enzymology/pathology; Metabolic Diseases/*genetics/metabolism; Mice
Creator
An entity primarily responsible for making the resource
Ferrell Jessica M; Boehme Shannon; Li Feng; Chiang John Y L
Description
An account of the resource
Cholesterol 7alpha-hydroxylase (CYP7A1) is the first and rate-limiting enzyme in the conversion of cholesterol to bile acids in the liver. In addition to absorption and digestion of nutrients, bile acids play a critical role in the regulation of lipid, glucose, and energy homeostasis. We have backcrossed Cyp7a1(-/-) mice in a mixed B6/129Sv genetic background to C57BL/6J mice to generate Cyp7a1(-/-) mice in a near-pure C57BL/6J background. These mice survive well and have normal growth and a bile acid pool size approximately 60% of WT mice. The expression of the genes in the alternative bile acid synthesis pathway are upregulated, resulting in a more hydrophilic bile acid composition with reduced cholic acid (CA). Surprisingly, Cyp7a1(-/-) mice have improved glucose sensitivity with reduced liver triglycerides and fecal bile acid excretion, but increased fecal fatty acid excretion and respiratory exchange ratio (RER) when fed a high-fat/high-cholesterol diet. Supplementing chow and Western diets with CA restored bile acid composition, reversed the glucose tolerant phenotype, and reduced the RER. Our current study points to a critical role of bile acid composition, rather than bile acid pool size, in regulation of glucose, lipid, and energy metabolism to improve glucose and insulin tolerance, maintain metabolic homeostasis, and prevent high-fat diet-induced metabolic disorders.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1194/jlr.M064709" target="_blank" rel="noreferrer noopener">10.1194/jlr.M064709</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*bile acids and salt/metabolism
*cholesterol/diet
*Lipids
*Liver
2016
Animal
Animals
Bile Acids and Salts/genetics/metabolism
Boehme Shannon
Chiang John Y L
Cholesterol 7-alpha-Hydroxylase/*genetics/metabolism
Cholesterol/*metabolism
Department of Integrative Medical Sciences
Diet
Disease Models
Exhalation/genetics
Ferrell Jessica M
Glucose/metabolism
High-Fat
Homeostasis
Humans
Journal of lipid research
Li Feng
Lipid Metabolism/genetics
Liver/enzymology/pathology
Metabolic Diseases/*genetics/metabolism
Mice
NEOMED College of Medicine
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1039/c6nr00398b" target="_blank" rel="noreferrer noopener">http://doi.org/10.1039/c6nr00398b</a>
Pages
6542–6554
Issue
12
Volume
8
Dublin Core
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Title
A name given to the resource
Anti-atherogenic effect of trivalent chromium-loaded CPMV nanoparticles in human aortic smooth muscle cells under hyperglycemic conditions in vitro.
Publisher
An entity responsible for making the resource available
Nanoscale
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-03
Subject
The topic of the resource
*Comovirus; Aorta/*metabolism; Atherosclerosis/*drug therapy/therapy; Azo Compounds/chemistry; Cell Proliferation; Cells; Chlorides/*chemistry; Chromium Compounds/*chemistry; Cultured; Cytokines/metabolism; Drug Delivery Systems; Electron; Fluorescence; Glucose/chemistry; Humans; Hyperglycemia/*metabolism; Lipids/chemistry; Microscopy; Myocytes; Nanoparticles/chemistry; NF-kappa B/metabolism; Proliferating Cell Nuclear Antigen/chemistry; Smooth Muscle/*metabolism; Spectrophotometry; Transforming Growth Factor beta/metabolism; Transmission; Ultraviolet
Creator
An entity primarily responsible for making the resource
Ganguly Rituparna; Wen Amy M; Myer Ashley B; Czech Tori; Sahu Soumyadip; Steinmetz Nicole F; Raman Priya
Description
An account of the resource
Atherosclerosis, a major macrovascular complication associated with diabetes, poses a tremendous burden on national health care expenditure. Despite extensive efforts, cost-effective remedies are unknown. Therapies for atherosclerosis are challenged by a lack of targeted drug delivery approaches. Toward this goal, we turn to a biology-derived drug delivery system utilizing nanoparticles formed by the plant virus, Cowpea mosaic virus (CPMV). The aim herein is to investigate the anti-atherogenic potential of the beneficial mineral nutrient, trivalent chromium, loaded CPMV nanoparticles in human aortic smooth muscle cells (HASMC) under hyperglycemic conditions. A non-covalent loading protocol is established yielding CrCl3-loaded CPMV (CPMV-Cr) carrying 2000 drug molecules per particle. Using immunofluorescence microscopy, we show that CPMV-Cr is readily taken up by HASMC in vitro. In glucose (25 mM)-stimulated cells, 100 nM CPMV-Cr inhibits HASMC proliferation concomitant to attenuated proliferating cell nuclear antigen (PCNA, proliferation marker) expression. This is accompanied by attenuation in high glucose-induced phospho-p38 and pAkt expression. Moreover, CPMV-Cr inhibits the expression of pro-inflammatory cytokines, transforming growth factor-beta (TGF-beta) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB), in glucose-stimulated HASMCs. Finally glucose-stimulated lipid uptake is remarkably abrogated by CPMV-Cr, revealed by Oil Red O staining. Together, these data provide key cellular evidence for an atheroprotective effect of CPMV-Cr in vascular smooth muscle cells (VSMC) under hyperglycemic conditions that may promote novel therapeutic ventures for diabetic atherosclerosis.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1039/c6nr00398b" target="_blank" rel="noreferrer noopener">10.1039/c6nr00398b</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Comovirus
2016
Aorta/*metabolism
Atherosclerosis/*drug therapy/therapy
Azo Compounds/chemistry
Cell Proliferation
Cells
Chlorides/*chemistry
Chromium Compounds/*chemistry
Cultured
Cytokines/metabolism
Czech Tori
Department of Integrative Medical Sciences
Drug Delivery Systems
Electron
Fluorescence
Ganguly Rituparna
Glucose/chemistry
Humans
Hyperglycemia/*metabolism
Lipids/chemistry
Microscopy
Myer Ashley B
Myocytes
Nanoparticles/chemistry
Nanoscale
NEOMED College of Medicine
NF-kappa B/metabolism
Proliferating Cell Nuclear Antigen/chemistry
Raman Priya
Sahu Soumyadip
Smooth Muscle/*metabolism
Spectrophotometry
Steinmetz Nicole F
Transforming Growth Factor beta/metabolism
Transmission
Ultraviolet
Wen Amy M
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1007/s00395-016-0547-4" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s00395-016-0547-4</a>
Pages
29–29
Issue
3
Volume
111
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Impaired coronary metabolic dilation in the metabolic syndrome is linked to mitochondrial dysfunction and mitochondrial DNA damage.
Publisher
An entity responsible for making the resource available
Basic research in cardiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-05
Subject
The topic of the resource
Animal; Animals; Coronary circulation; Coronary microcirculation; Coronary Vessels/metabolism/*physiopathology; Diabetes; Disease Models; DNA; DNA Damage/physiology; DNA Fragmentation; Metabolic Syndrome/metabolism/*physiopathology; Mitochondria; Mitochondria/*metabolism; Mitochondrial/*metabolism; Obesity; Oxidative Stress/physiology; Rats; Reactive Oxygen Species/metabolism; Vasodilation/physiology; Zucker
Creator
An entity primarily responsible for making the resource
Guarini Giacinta; Kiyooka Takahiko; Ohanyan Vahagn; Pung Yuh Fen; Marzilli Mario; Chen Yeong-Renn; Chen Chwen-Lih; Kang Patrick T; Hardwick James P; Kolz Christopher L; Yin Liya; Wilson Glenn L; Shokolenko Inna; Dobson James G Jr; Fenton Richard; Chilian William M
Description
An account of the resource
Mitochondrial dysfunction in obesity and diabetes can be caused by excessive production of free radicals, which can damage mitochondrial DNA. Because mitochondrial DNA plays a key role in the production of ATP necessary for cardiac work, we hypothesized that mitochondrial dysfunction, induced by mitochondrial DNA damage, uncouples coronary blood flow from cardiac work. Myocardial blood flow (contrast echocardiography) was measured in Zucker lean (ZLN) and obese fatty (ZOF) rats during increased cardiac metabolism (product of heart rate and arterial pressure, i.v. norepinephrine). In ZLN increased metabolism augmented coronary blood flow, but in ZOF metabolic hyperemia was attenuated. Mitochondrial respiration was impaired and ROS production was greater in ZOF than ZLN. These were associated with mitochondrial DNA (mtDNA) damage in ZOF. To determine if coronary metabolic dilation, the hyperemic response induced by heightened cardiac metabolism, is linked to mitochondrial function we introduced recombinant proteins (intravenously or intraperitoneally) in ZLN and ZOF to fragment or repair mtDNA, respectively. Repair of mtDNA damage restored mitochondrial function and metabolic dilation, and reduced ROS production in ZOF; whereas induction of mtDNA damage in ZLN reduced mitochondrial function, increased ROS production, and attenuated metabolic dilation. Adequate metabolic dilation was also associated with the extracellular release of ADP, ATP, and H2O2 by cardiac myocytes; whereas myocytes from rats with impaired dilation released only H2O2. In conclusion, our results suggest that mitochondrial function plays a seminal role in connecting myocardial blood flow to metabolism, and integrity of mtDNA is central to this process.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1007/s00395-016-0547-4" target="_blank" rel="noreferrer noopener">10.1007/s00395-016-0547-4</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2016
Animal
Animals
Basic research in cardiology
Chen Chwen-Lih
Chen Yeong-Renn
Chilian William M
Coronary Circulation
Coronary microcirculation
Coronary Vessels/metabolism/*physiopathology
Department of Integrative Medical Sciences
Diabetes
Disease Models
DNA
DNA Damage/physiology
DNA Fragmentation
Dobson James G Jr
Fenton Richard
Guarini Giacinta
Hardwick James P
Kang Patrick T
Kiyooka Takahiko
Kolz Christopher L
Marzilli Mario
Metabolic Syndrome/metabolism/*physiopathology
Mitochondria
Mitochondria/*metabolism
Mitochondrial/*metabolism
NEOMED College of Medicine
Obesity
Ohanyan Vahagn
Oxidative Stress/physiology
Pung Yuh Fen
Rats
Reactive Oxygen Species/metabolism
Shokolenko Inna
Vasodilation/physiology
Wilson Glenn L
Yin Liya
Zucker
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.jaci.2015.06.030" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.jaci.2015.06.030</a>
Pages
289–298
Issue
1
Volume
137
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Leukotriene D4 and prostaglandin E2 signals synergize and potentiate vascular inflammation in a mast cell-dependent manner through cysteinyl leukotriene receptor 1 and E-prostanoid receptor 3.
Publisher
An entity responsible for making the resource available
The Journal of allergy and clinical immunology
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-01
Subject
The topic of the resource
Animals; c-fos; Capillary Permeability; Cell Line; CysLT(1)R; Dinoprostone/*immunology; E-prostanoid receptor 3; Edema/immunology; EP3 Subtype/*immunology; extracellular signal-regulated kinase; Humans; Inbred BALB C; Inbred C57BL; Inflammation/immunology; leukotriene D(4); Leukotriene D4/*immunology; Leukotriene/*immunology; macrophage inflammatory protein 1beta; Mast cells; Mast Cells/*immunology; Mice; prostaglandin D(2); Prostaglandin E; prostaglandin E(2); protein kinase G; Receptors; Transgenic; Tumor
Creator
An entity primarily responsible for making the resource
Kondeti Vinay; Al-Azzam Nosayba; Duah Ernest; Thodeti Charles K; Boyce Joshua A; Paruchuri Sailaja
Description
An account of the resource
BACKGROUND: Although arachidonic acid metabolites, cysteinyl leukotrienes (cys-LTs; leukotriene [LT] C4, LTD4, and LTE4), and prostaglandin (PG) E2 are generated at the site of inflammation, it is not known whether crosstalk exists between these 2 classes of inflammatory mediators. OBJECTIVE: We sought to determine the role of LTD4-PGE2 crosstalk in inducing vascular inflammation in vivo, identify effector cells, and ascertain specific receptors and pathways involved in vitro. METHODS: Vascular (ear) inflammation was assessed by injecting agonists into mouse ears, followed by measuring ear thickness and histology, calcium influx with Fura-2, phosphorylation and expression of signaling molecules by means of immunoblotting, PGD2 and macrophage inflammatory protein 1beta generation by using ELISA, and expression of transcripts by using RT-PCR. Candidate receptors and signaling molecules were identified by using antagonists and inhibitors and confirmed by using small interfering RNA. RESULTS: LTD4 plus PGE2 potentiated vascular permeability and edema, gearing the system toward proinflammation in wild-type mice but not in Kit(W-sh) mice. Furthermore, LTD4 plus PGE2, through cysteinyl leukotriene receptor 1 (CysLT1R) and E-prostanoid receptor (EP) 3, enhanced extracellular signal-regulated kinase (Erk) and c-fos phosphorylation, inflammatory gene expression, macrophage inflammatory protein 1beta secretion, COX-2 upregulation, and PGD2 generation in mast cells. Additionally, we uncovered that this synergism is mediated through Gi, protein kinase G, and Erk signaling. LTD4 plus PGE2-potentiated effects are partially sensitive to CysLT1R or EP3 antagonists but completely abolished by simultaneous treatment both in vitro and in vivo. CONCLUSIONS: Our results unravel a unique
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.jaci.2015.06.030" target="_blank" rel="noreferrer noopener">10.1016/j.jaci.2015.06.030</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2016
Al-Azzam Nosayba
Animals
Boyce Joshua A
c-fos
Capillary Permeability
Cell Line
CysLT(1)R
Department of Integrative Medical Sciences
Dinoprostone/*immunology
Duah Ernest
E-prostanoid receptor 3
Edema/immunology
EP3 Subtype/*immunology
extracellular signal-regulated kinase
Humans
Inbred BALB C
Inbred C57BL
Inflammation/immunology
Kondeti Vinay
leukotriene D(4)
Leukotriene D4/*immunology
Leukotriene/*immunology
macrophage inflammatory protein 1beta
Mast cells
Mast Cells/*immunology
Mice
NEOMED College of Medicine
Paruchuri Sailaja
prostaglandin D(2)
Prostaglandin E
prostaglandin E(2)
protein kinase G
Receptors
The Journal of allergy and clinical immunology
Thodeti Charles K
Transgenic
Tumor
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.canlet.2016.05.014" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.canlet.2016.05.014</a>
Pages
131–141
Issue
2
Volume
378
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Lipopolysaccharide supports maintaining the stemness of CD133(+) hepatoma cells through activation of the NF-kappaB/HIF-1alpha pathway.
Publisher
An entity responsible for making the resource available
Cancer letters
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-08
Subject
The topic of the resource
*Cancer stem cells; *Lipopolysaccharide; *Plasticity; *Stemness maintenance; *Tumor microenvironment; AC133 Antigen/genetics/*metabolism; alpha Subunit/genetics/*metabolism; Animals; Antineoplastic Agents – Pharmacodynamics; Antineoplastic Agents/pharmacology; Body Weights and Measures; Carcinoma; Cell Line; Cell Movement – Drug Effects; Cell Movement/drug effects; Cell Physiology; Cell Physiology – Drug Effects; Cell Proliferation/drug effects; Drug Resistance; Gene Expression Regulation; Genes; Genetic Techniques; Hepatocellular; Hepatocellular – Drug Therapy; Hepatocellular – Metabolism; Hepatocellular – Pathology; Hepatocellular/drug therapy/genetics/*metabolism/pathology; Humans; Hypoxia-Inducible Factor 1; Inbred BALB C; Lipopolysaccharides – Pharmacodynamics; Lipopolysaccharides/*pharmacology; Liver Neoplasms; Liver Neoplasms – Drug Therapy; Liver Neoplasms – Metabolism; Liver Neoplasms – Pathology; Liver Neoplasms/drug therapy/genetics/*metabolism/pathology; Male; Mice; Neoplasm; Neoplasm Invasiveness; Neoplastic; Neoplastic Stem Cells/*drug effects/metabolism/pathology; NF-kappa B – Metabolism; NF-kappa B/*metabolism; Nude; Phenotype; Proteins; Proteins – Metabolism; RNA Interference; Signal Transduction – Drug Effects; Signal Transduction/drug effects; Stem Cells – Drug Effects; Stem Cells – Metabolism; Stem Cells – Pathology; Time Factors; Transfection; Tumor Burden; Tumor Microenvironment
Creator
An entity primarily responsible for making the resource
Lai Fo-Bao; Liu Wen-Ting; Jing Ying-Ying; Yu Guo-Feng; Han Zhi-Peng; Yang Xue; Zeng Jian-Xing; Zhang Hang-Jie; Shi Rong-Yu; Li Xiao-Yong; Pan Xiao-Rong; Li Rong; Zhao Qiu-Dong; Wu Meng-Chao; Zhang Ping; Liu Jing-Feng; Wei Li-Xin
Description
An account of the resource
Due to the existence of cancer stem cells (CSCs), persistence and relapse of human hepatocellular carcinoma (HCC) are common after treatment with existing anti-cancer therapies. Emerging evidence indicates that lipopolysaccharide (LPS) plays a crucial role in aggravating HCC, but information about the effect of LPS on CSCs of HCC remains scant. Here, we report that the stemness of CD133(+) CSCs sorted from the human HCC cell line Huh7 was maintained well when cells were cultured with LPS. The reduction of CD133 expression was much lesser in cultured CSCs in the presence of LPS. In response to LPS stimulation, CSCs showed an increase in their activity of clonogenesis and tumorigenesis. LPS also supported maintaining CSC abilities of migration, invasion, and chemo-resistance. Treatment with HIF-1alpha-specific siRNA significantly reduced CD133 expression by CSCs at both mRNA and protein levels. Further, the expression of HIF-1alpha and CD133 was reduced in LPS-stimulated CSCs when the NF-kappaB inhibitor was added to the cell culture. HIF-1alpha-specific siRNA also effectively counteracted the effect of LPS on maintaining CSC abilities of migration and invasion. These data indicate that LPS, an important mediator in the liver tumor microenvironment, supports the maintenance of CSC stemness through signaling of the NF-kappaB/HIF-1alpha pathway. Our current study highlights LPS as a potential target for developing new therapeutic approaches to eliminate CSCs during the treatment of HCC.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.canlet.2016.05.014" target="_blank" rel="noreferrer noopener">10.1016/j.canlet.2016.05.014</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Cancer stem cells
*Lipopolysaccharide
*Plasticity
*Stemness maintenance
*Tumor microenvironment
2016
AC133 Antigen/genetics/*metabolism
alpha Subunit/genetics/*metabolism
Animals
Antineoplastic Agents – Pharmacodynamics
Antineoplastic Agents/pharmacology
Body Weights and Measures
Cancer letters
Carcinoma
Cell Line
Cell Movement – Drug Effects
Cell Movement/drug effects
Cell Physiology
Cell Physiology – Drug Effects
Cell Proliferation/drug effects
Department of Integrative Medical Sciences
Drug Resistance
Gene Expression Regulation
Genes
Genetic Techniques
Han Zhi-Peng
Hepatocellular
Hepatocellular – Drug Therapy
Hepatocellular – Metabolism
Hepatocellular – Pathology
Hepatocellular/drug therapy/genetics/*metabolism/pathology
Humans
Hypoxia-Inducible Factor 1
Inbred BALB C
Jing Ying-Ying
Lai Fo-Bao
Li Rong
Li Xiao-Yong
Lipopolysaccharides – Pharmacodynamics
Lipopolysaccharides/*pharmacology
Liu Jing-Feng
Liu Wen-Ting
Liver Neoplasms
Liver Neoplasms – Drug Therapy
Liver Neoplasms – Metabolism
Liver Neoplasms – Pathology
Liver Neoplasms/drug therapy/genetics/*metabolism/pathology
Male
Mice
NEOMED College of Medicine
Neoplasm
Neoplasm Invasiveness
Neoplastic
Neoplastic Stem Cells/*drug effects/metabolism/pathology
NF-kappa B – Metabolism
NF-kappa B/*metabolism
Nude
Pan Xiao-Rong
Phenotype
Proteins
Proteins – Metabolism
RNA Interference
Shi Rong-Yu
Signal Transduction – Drug Effects
Signal Transduction/drug effects
Stem Cells – Drug Effects
Stem Cells – Metabolism
Stem Cells – Pathology
Time Factors
Transfection
Tumor Burden
Tumor Microenvironment
Wei Li-Xin
Wu Meng-Chao
Yang Xue
Yu Guo-Feng
Zeng Jian-Xing
Zhang Hang-Jie
Zhang Ping
Zhao Qiu-Dong
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1128/JVI.03156-15" target="_blank" rel="noreferrer noopener">http://doi.org/10.1128/JVI.03156-15</a>
Pages
3385–3399
Issue
7
Volume
90
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Ecotropic Murine Leukemia Virus Infection of Glial Progenitors Interferes with Oligodendrocyte Differentiation: Implications for Neurovirulence.
Publisher
An entity responsible for making the resource available
Journal of virology
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-01
Subject
The topic of the resource
3T3 Cells; Animals; Cell Line; Cell Proliferation; Cell Survival; env/biosynthesis; Female; Gene Products; Leukemia Virus; Male; Mice; Motor Neuron Disease/*virology; Murine/*pathogenicity; Neural Stem Cells/*virology; Neurogenesis/*physiology; Neuroglia/*virology; Oligodendroglia/cytology/virology; Retroviridae Infections/*complications; Transgenic
Creator
An entity primarily responsible for making the resource
Li Ying; Dunphy Jaclyn M; Pedraza Carlos E; Lynch Connor R; Cardona Sandra M; Macklin Wendy B; Lynch William P
Description
An account of the resource
UNLABELLED: Certain murine leukemia viruses (MLVs) are capable of inducing fatal progressive spongiform motor neuron disease in mice that is largely mediated by viral Env glycoprotein expression within central nervous system (CNS) glia. While the etiologic mechanisms and the glial subtypes involved remain unresolved, infection of NG2 glia was recently observed to correlate spatially and temporally with altered neuronal physiology and spongiogenesis. Since one role of NG2 cells is to serve as oligodendrocyte (OL) progenitor cells (OPCs), we examined here whether their infection by neurovirulent (FrCasE) or nonneurovirulent (Fr57E) ecotropic MLVs influenced their viability and/or differentiation. Here, we demonstrate that OPCs, but not OLs, are major CNS targets of both FrCasE and Fr57E. We also show that MLV infection of neural progenitor cells (NPCs) in culture did not affect survival, proliferation, or OPC progenitor marker expression but suppressed certain glial differentiation markers. Assessment of glial differentiation in vivo using transplanted transgenic NPCs showed that, while MLVs did not affect cellular engraftment or survival, they did inhibit OL differentiation, irrespective of MLV neurovirulence. In addition, in chimeric brains, where FrCasE-infected NPC transplants caused neurodegeneration, the transplanted NPCs proliferated. These results suggest that MLV infection is not directly cytotoxic to OPCs but rather acts to interfere with OL differentiation. Since both FrCasE and Fr57E viruses restrict OL differentiation but only FrCasE induces overt neurodegeneration, restriction of OL maturation alone cannot account for neuropathogenesis. Instead neurodegeneration may involve a two-hit scenario where interference with OPC differentiation combined with glial Env-induced neuronal hyperexcitability precipitates disease. IMPORTANCE: A variety of human and animal retroviruses are capable of causing central nervous system (CNS) neurodegeneration manifested as motor and cognitive deficits. These retroviruses infect a variety of CNS cell types; however, the specific role each cell type plays in neuropathogenesis remains to be established. The NG2 glia, whose CNS functions are only now emerging, are a newly appreciated viral target in murine leukemia virus (MLV)-induced neurodegeneration. Since one role of NG2 glia is that of oligodendrocyte progenitor cells (OPCs), we investigated here whether their infection by the neurovirulent MLV FrCasE contributed to neurodegeneration by affecting OPC viability and/or development. Our results show that both neurovirulent and nonneurovirulent MLVs interfere with oligodendrocyte differentiation. Thus, NG2 glial infection could contribute to neurodegeneration by preventing myelin formation and/or repair and by suspending OPCs in a state of persistent susceptibility to excitotoxic insult mediated by neurovirulent virus effects on other glial subtypes.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1128/JVI.03156-15" target="_blank" rel="noreferrer noopener">10.1128/JVI.03156-15</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2016
3T3 Cells
Animals
Cardona Sandra M
Cell Line
Cell Proliferation
Cell Survival
Department of Integrative Medical Sciences
Dunphy Jaclyn M
env/biosynthesis
Female
Gene Products
Journal of virology
Leukemia Virus
Li Ying
Lynch Connor R
Lynch William P
Macklin Wendy B
Male
Mice
Motor Neuron Disease/*virology
Murine/*pathogenicity
NEOMED College of Medicine
Neural Stem Cells/*virology
Neurogenesis/*physiology
Neuroglia/*virology
Oligodendroglia/cytology/virology
Pedraza Carlos E
Retroviridae Infections/*complications
Transgenic
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1002/hep.28472" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/hep.28472</a>
Pages
1860–1874
Issue
6
Volume
63
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Carboxylesterase 2 prevents liver steatosis by modulating lipolysis, endoplasmic reticulum stress, and lipogenesis and is regulated by hepatocyte nuclear factor 4 alpha in mice.
Publisher
An entity responsible for making the resource available
Hepatology (Baltimore, Md.)
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-06
Subject
The topic of the resource
*Lipid Metabolism; Adiposity; Animals; Carboxylesterase/*metabolism; Carboxylic Ester Hydrolases/genetics/*metabolism; Diabetes Mellitus; Diet; Endoplasmic Reticulum Stress; Energy Metabolism; Experimental/enzymology; Gene Knockdown Techniques; Glucose Tolerance Test; Glucose/metabolism; Hepatocyte Nuclear Factor 4/*metabolism; High-Fat/adverse effects; Homeostasis; Humans; Inbred C57BL; Lipogenesis; Lipolysis; Liver/enzymology; Male; Mice; Non-alcoholic Fatty Liver Disease/*etiology/metabolism; Obesity/enzymology/etiology; Sterol Regulatory Element Binding Protein 1/metabolism
Creator
An entity primarily responsible for making the resource
Li Yuanyuan; Zalzala Munaf; Jadhav Kavita; Xu Yang; Kasumov Takhar; Yin Liya; Zhang Yanqiao
Description
An account of the resource
UNLABELLED: Nonalcoholic fatty liver disease (NAFLD) is a common liver disease that ranges from simple steatosis to nonalcoholic steatohepatitis (NASH). So far, the underlying mechanism remains poorly understood. Here, we show that hepatic carboxylesterase 2 (CES2) is markedly reduced in NASH patients, diabetic db/db mice, and high-fat diet (HFD)-fed mice. Restoration of hepatic CES2 expression in db/db or HFD-fed mice markedly ameliorates liver steatosis and insulin resistance. In contrast, knockdown of hepatic CES2 causes liver steatosis and damage in chow- or Western diet-fed C57BL/6 mice. Mechanistically, we demonstrate that CES2 has triglyceride hydrolase activity. As a result, gain of hepatic CES2 function increases fatty acid oxidation and inhibits lipogenesis, whereas loss of hepatic CES2 stimulates lipogenesis by inducing endoplasmic reticulum stress. We further show that loss of hepatic CES2 stimulates lipogenesis in a sterol regulatory element-binding protein 1 (SREBP-1)-dependent manner. Finally, we show that hepatocyte nuclear factor 4 alpha (HNF-4alpha) plays a key role in controlling hepatic CES2 expression in diabetes, obesity, or NASH. CONCLUSION: CES2 plays a protective role in development of NAFLD. Targeting the
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1002/hep.28472" target="_blank" rel="noreferrer noopener">10.1002/hep.28472</a>
Rights
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Lipid Metabolism
2016
Adiposity
Animals
Carboxylesterase/*metabolism
Carboxylic Ester Hydrolases/genetics/*metabolism
Department of Integrative Medical Sciences
Department of Pharmaceutical Sciences
Diabetes Mellitus
Diet
Endoplasmic Reticulum Stress
Energy Metabolism
Experimental/enzymology
Gene Knockdown Techniques
Glucose Tolerance Test
Glucose/metabolism
Hepatocyte Nuclear Factor 4/*metabolism
Hepatology (Baltimore, Md.)
High-Fat/adverse effects
Homeostasis
Humans
Inbred C57BL
Jadhav Kavita
Kasumov Takhar
Li Yuanyuan
Lipogenesis
Lipolysis
Liver/enzymology
Male
Mice
NEOMED College of Medicine
NEOMED College of Pharmacy
Non-alcoholic Fatty Liver Disease/*etiology/metabolism
Obesity/enzymology/etiology
Sterol Regulatory Element Binding Protein 1/metabolism
Xu Yang
Yin Liya
Zalzala Munaf
Zhang Yanqiao
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1194/jlr.M069807" target="_blank" rel="noreferrer noopener">http://doi.org/10.1194/jlr.M069807</a>
Pages
1831–1844
Issue
10
Volume
57
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Cholesterol 7alpha-hydroxylase protects the liver from inflammation and fibrosis by maintaining cholesterol homeostasis.
Publisher
An entity responsible for making the resource available
Journal of lipid research
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-10
Subject
The topic of the resource
*bile acid; *Cholesterol 7-alpha-Hydroxylase/genetics/metabolism; *farnesoid X receptor; *Homeostasis; *Liver Cirrhosis/chemically induced/enzymology/genetics/prevention & control; *Liver/enzymology/pathology; *nuclear receptor; *Takeda G protein-coupled receptor 5; Animals; Cholesterol/genetics/*metabolism; G-Protein-Coupled/genetics/metabolism; Hep G2 Cells; Humans; Knockout; Mice; NF-kappa B/genetics/metabolism; Oxidative Stress; Receptors; Tumor Necrosis Factor-alpha/genetics/metabolism
Creator
An entity primarily responsible for making the resource
Liu Hailiang; Pathak Preeti; Boehme Shannon; Chiang John Y L
Description
An account of the resource
Cholesterol 7alpha-hydroxylase (CYP7A1) plays a critical role in control of bile acid and cholesterol homeostasis. Bile acids activate farnesoid X receptor (FXR) and Takeda G protein-coupled receptor 5 (TGR5) to regulate lipid, glucose, and energy metabolism. However, the role of bile acids in hepatic inflammation and fibrosis remains unclear. In this study, we showed that adenovirus-mediated overexpression of Cyp7a1 ameliorated lipopolysaccharide (LPS)-induced inflammatory cell infiltration and pro-inflammatory cytokine production in WT and
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1194/jlr.M069807" target="_blank" rel="noreferrer noopener">10.1194/jlr.M069807</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*bile acid
*Cholesterol 7-alpha-Hydroxylase/genetics/metabolism
*Farnesoid X receptor
*Homeostasis
*Liver Cirrhosis/chemically induced/enzymology/genetics/prevention & control
*Liver/enzymology/pathology
*nuclear receptor
*Takeda G protein-coupled receptor 5
2016
Animals
Boehme Shannon
Chiang John Y L
Cholesterol/genetics/*metabolism
Department of Integrative Medical Sciences
G-Protein-Coupled/genetics/metabolism
Hep G2 Cells
Humans
Journal of lipid research
Knockout
Liu Hailiang
Mice
NEOMED College of Medicine
NF-kappa B/genetics/metabolism
Oxidative Stress
Pathak Preeti
Receptors
Tumor Necrosis Factor-alpha/genetics/metabolism
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1152/ajpheart.00449.2015" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00449.2015</a>
Pages
H20–28
Issue
1
Volume
310
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Early upregulation of myocardial CXCR4 expression is critical for dimethyloxalylglycine-induced cardiac improvement in acute myocardial infarction.
Publisher
An entity responsible for making the resource available
American journal of physiology. Heart and circulatory physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-01
Subject
The topic of the resource
alpha Subunit/metabolism; Amino Acids; Animal; Animals; Apoptosis/drug effects; Cardiotonic Agents/*pharmacology; Cell Hypoxia; Cell Line; CXCR4/deficiency/genetics/*metabolism; Dicarboxylic/*pharmacology; Disease Models; Enzyme Inhibitors/pharmacology; hypoxia; Hypoxia-Inducible Factor 1; Hypoxia-Inducible Factor-Proline Dioxygenases/antagonists & inhibitors/metabolism; Inbred C57BL; Knockout; Left/*drug effects; Mice; myocardial infarction; Myocardial Infarction/*drug therapy/genetics/metabolism/pathology/physiopathology; Myocardium/*metabolism/pathology; Rats; Receptors; Recovery of Function; Signal Transduction/drug effects; stem cells; Stem Cells/drug effects/metabolism; Stroke Volume/drug effects; Time Factors; Up-Regulation; Ventricular Function
Creator
An entity primarily responsible for making the resource
Mayorga Mari; Kiedrowski Matthew; Shamhart Patricia; Forudi Farhad; Weber Kristal; Chilian William M; Penn Marc S; Dong Feng
Description
An account of the resource
The stromal cell-derived factor-1 (SDF-1):CXCR4 is important in myocardial repair. In this study we tested the hypothesis that early upregulation of cardiomyocyte CXCR4 (CM-CXCR4) at a time of high myocardial SDF-1 expression could be a strategy to engage the SDF-1:CXCR4 axis and improve cardiac repair. The effects of the hypoxia inducible factor (HIF) hydroxylase inhibitor dimethyloxalylglycine (DMOG) on CXCR4 expression was tested on H9c2 cells. In mice a myocardial infarction (MI) was produced in CM-CXCR4 null and wild-type controls. Mice were randomized to receive injection of DMOG (DMOG group) or saline (Saline group) into the border zone after MI. Protein and mRNA expression of CM-CXCR4 were quantified. Echocardiography was used to assess cardiac function. During hypoxia, DMOG treatment increased CXCR4 expression of H9c2 cells by 29 and 42% at 15 and 24 h, respectively. In vivo DMOG treatment increased
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.00449.2015" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00449.2015</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2016
alpha Subunit/metabolism
American journal of physiology. Heart and circulatory physiology
Amino Acids
Animal
Animals
Apoptosis/drug effects
Cardiotonic Agents/*pharmacology
Cell Hypoxia
Cell Line
Chilian William M
CXCR4/deficiency/genetics/*metabolism
Department of Integrative Medical Sciences
Dicarboxylic/*pharmacology
Disease Models
Dong Feng
Enzyme Inhibitors/pharmacology
Forudi Farhad
hypoxia
Hypoxia-Inducible Factor 1
Hypoxia-Inducible Factor-Proline Dioxygenases/antagonists & inhibitors/metabolism
Inbred C57BL
Kiedrowski Matthew
Knockout
Left/*drug effects
Mayorga Mari
Mice
myocardial infarction
Myocardial Infarction/*drug therapy/genetics/metabolism/pathology/physiopathology
Myocardium/*metabolism/pathology
NEOMED College of Medicine
Penn Marc S
Rats
Receptors
Recovery of Function
Shamhart Patricia
Signal Transduction/drug effects
stem cells
Stem Cells/drug effects/metabolism
Stroke Volume/drug effects
Time Factors
Up-Regulation
Ventricular Function
Weber Kristal
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1194/jlr.M069013" target="_blank" rel="noreferrer noopener">http://doi.org/10.1194/jlr.M069013</a>
Pages
1541–1551
Issue
8
Volume
57
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Cholesteryl ester transfer protein alters liver and plasma triglyceride metabolism through two liver networks in female mice.
Publisher
An entity responsible for making the resource available
Journal of lipid research
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-08
Subject
The topic of the resource
*estrogen; *estrogen receptor alpha; *lipid and lipoprotein metabolism; *small heterodimer partner; *triglycerides; *very low density lipoprotein; Animals; Cholesterol Ester Transfer Proteins/*physiology; Estrogen Receptor alpha/metabolism; Estrogens/physiology; Female; Inbred C57BL; Lipid Metabolism; Liver/*metabolism; Metabolic Networks and Pathways; Mice; Oxidation-Reduction; Transgenic; Triglycerides/biosynthesis/*blood
Creator
An entity primarily responsible for making the resource
Palmisano Brian T; Le Thao D; Zhu Lin; Lee Yoon-Kwang; Stafford John M
Description
An account of the resource
Elevated plasma TGs increase risk of cardiovascular disease in women. Estrogen treatment raises plasma TGs in women, but molecular mechanisms remain poorly understood. Here we explore the role of cholesteryl ester transfer protein (CETP) in the regulation of TG metabolism in female mice, which naturally lack CETP. In transgenic CETP females, acute estrogen treatment raised plasma TGs 50%, increased TG production, and increased expression of genes involved in VLDL synthesis, but not in nontransgenic littermate females. In CETP females, estrogen enhanced expression of small heterodimer partner (SHP), a nuclear receptor regulating VLDL production. Deletion of liver SHP prevented increases in TG production and expression of genes involved in VLDL synthesis in CETP mice with estrogen treatment. We also examined whether CETP expression had effects on TG metabolism independent of estrogen treatment. CETP increased liver beta-oxidation and reduced liver TG content by 60%. Liver estrogen receptor alpha (ERalpha) was required for CETP expression to enhance beta-oxidation and reduce liver TG content. Thus, CETP alters at least two networks governing TG metabolism, one involving SHP to increase VLDL-TG production in response to estrogen, and another involving ERalpha to enhance beta-oxidation and lower liver TG content. These findings demonstrate a novel role for CETP in estrogen-mediated increases in TG production and a broader role for CETP in TG metabolism.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1194/jlr.M069013" target="_blank" rel="noreferrer noopener">10.1194/jlr.M069013</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*estrogen
*estrogen receptor alpha
*lipid and lipoprotein metabolism
*small heterodimer partner
*triglycerides
*very low density lipoprotein
2016
Animals
Cholesterol Ester Transfer Proteins/*physiology
Department of Integrative Medical Sciences
Estrogen Receptor alpha/metabolism
Estrogens/physiology
Female
Inbred C57BL
Journal of lipid research
Le Thao D
Lee Yoon-Kwang
Lipid Metabolism
Liver/*metabolism
Metabolic Networks and Pathways
Mice
NEOMED College of Medicine
Oxidation-Reduction
Palmisano Brian T
Stafford John M
Transgenic
Triglycerides/biosynthesis/*blood
Zhu Lin
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1152/ajpgi.00343.2015" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpgi.00343.2015</a>
Pages
G799–807
Issue
10
Volume
310
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Enhanced ethanol catabolism in orphan nuclear receptor SHP-null mice.
Publisher
An entity responsible for making the resource available
American journal of physiology. Gastrointestinal and liver physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-05
Subject
The topic of the resource
*acetaldehyde dehydrogenase; *alcoholic fatty liver disease; *inflammation; *small heterodimer partner; Acetates/blood; Alcoholic/genetics/*metabolism; Aldehyde Dehydrogenase; Animals; Cytoplasmic and Nuclear/deficiency/*genetics/metabolism; Ethanol/blood/*metabolism/toxicity; Inbred C57BL; Lipid Peroxidation; Liver Diseases; Liver/drug effects/metabolism; Male; Mice; Mitochondrial/genetics/metabolism; PPAR gamma/genetics/metabolism; Receptors
Creator
An entity primarily responsible for making the resource
Park Jung Eun; Lee Mikang; Mifflin Ryan; Lee Yoon-Kwang
Description
An account of the resource
Deficiency of the orphan nuclear hormone receptor small heterodimer partner (SHP, NR0B2) protects mice from diet-induced hepatic steatosis, in part, via repression of peroxisome proliferator-activated receptor (PPAR)-gamma2 (Pparg2) gene expression. Alcoholic fatty liver diseases (AFLD) share many common pathophysiological features with non-AFLD. To study the role of SHP and PPARgamma2 in AFLD, we used a strategy of chronic ethanol feeding plus a single binge ethanol feeding to challenge wild-type (WT) and SHP-null (SHP(-/-)) mice with ethanol. The ethanol feeding induced liver fat accumulation and mRNA expression of hepatic Pparg2 in WT mice, which suggests that a high level of PPARgamma2 is a common driving force for fat accumulation induced by ethanol or a high-fat diet. Interestingly, ethanol-fed SHP(-/-) mice displayed hepatic fat accumulation similar to that of ethanol-fed WT mice, even though their Pparg2 expression level remained lower. Mortality of SHP(-/-) mice after ethanol binge feeding was significantly reduced and their acetaldehyde dehydrogenase (Aldh2) mRNA level was higher than that of their WT counterparts. After an intoxicating dose of ethanol, SHP(-/-) mice exhibited faster blood ethanol clearance and earlier wake-up time than WT mice. Higher blood acetate, the end product of ethanol metabolism, and lower acetaldehyde levels were evident in the ethanol-challenged SHP(-/-) than WT mice. Ethanol-induced inflammatory responses and lipid peroxidation were also lower in SHP(-/-) mice. The current data show faster ethanol catabolism and extra fat storage through conversion of acetate to acetyl-CoA before its release into the circulation in this ethanol-feeding model in SHP(-/-) mice.
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<a href="http://doi.org/10.1152/ajpgi.00343.2015" target="_blank" rel="noreferrer noopener">10.1152/ajpgi.00343.2015</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*acetaldehyde dehydrogenase
*alcoholic fatty liver disease
*Inflammation
*small heterodimer partner
2016
Acetates/blood
Alcoholic/genetics/*metabolism
Aldehyde Dehydrogenase
American journal of physiology. Gastrointestinal and liver physiology
Animals
Cytoplasmic and Nuclear/deficiency/*genetics/metabolism
Department of Integrative Medical Sciences
Ethanol/blood/*metabolism/toxicity
Inbred C57BL
Lee Mikang
Lee Yoon-Kwang
Lipid Peroxidation
Liver Diseases
Liver/drug effects/metabolism
Male
Mice
Mifflin Ryan
Mitochondrial/genetics/metabolism
NEOMED College of Medicine
Park Jung Eun
PPAR gamma/genetics/metabolism
Receptors
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1152/ajpcell.00068.2016" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpcell.00068.2016</a>
Pages
C212–224
Issue
2
Volume
311
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Leptin augments recruitment of IRF-1 and CREB to thrombospondin-1 gene promoter in vascular smooth muscle cells in vitro.
Publisher
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American journal of physiology. Cell physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-08
Subject
The topic of the resource
*cAMP response element-binding protein; *interferon regulatory factor-1; *leptin; *thrombospondin-1; *transcription; *vascular smooth muscle cells; Binding Sites/genetics; Cells; Chromatin Immunoprecipitation/methods; Cultured; Cyclic AMP Response Element-Binding Protein/*metabolism; Gene Expression Regulation/genetics; Genetic/genetics; Humans; Interferon Regulatory Factor-1/*metabolism; Leptin/*metabolism; Muscle; Mutagenesis; Myocytes; Promoter Regions; Response Elements/genetics; Site-Directed/methods; Smooth; Smooth Muscle/*metabolism; Thrombospondin 1/*genetics/*metabolism; Transcription; Transcriptional Activation/genetics; Transfection/methods; Up-Regulation/genetics; Vascular/*metabolism
Creator
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Sahu Soumyadip; Ganguly Rituparna; Raman Priya
Description
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We previously reported that high pathophysiological concentrations of leptin, the adipocyte-secreted peptide, upregulate the expression of a potent proatherogenic matricellular protein, thrombospondin-1 (TSP-1), in vascular smooth muscle cells. Moreover, this regulation was found to occur at the level of transcription; however, the underlying molecular mechanisms remain unknown. The goal of the present study was to investigate the specific transcriptional mechanisms that mediate upregulation of TSP-1 expression by leptin. Primary human aortic smooth muscle cell cultures were transiently transfected with different TSP-1 gene (THBS1) promoter-linked luciferase reporter constructs, and luciferase activity in response to leptin (100 ng/ml) was assessed. We identified a long THBS1 promoter (-1270/+750) fragment with specific leptin response elements that are required for increased TSP-1 transcription by leptin. Promoter analyses, protein/DNA array and gel shift assays demonstrated activation and association of transcription factors, interferon regulatory factor-1 (IRF-1) and cAMP response element-binding protein (CREB), to the distal fragment of the THBS1 promoter in response to leptin. Supershift, chromatin immunoprecipitation, and coimmunoprecipitation assays revealed formation of a single complex between IRF-1 and CREB in response to leptin; importantly, recruitment of this complex to the THBS1 promoter mediated leptin-induced TSP-1 transcription. Finally, binding sequence decoy oligomer and site-directed mutagenesis revealed that regulatory elements for both IRF-1 (-1019 to -1016) and CREB (-1198 to -1195), specific to the distal THBS1 promoter, were required for leptin-induced TSP-1 transcription. Taken together, these findings demonstrate that leptin promotes a cooperative association between IRF-1 and CREB on the THBS1 promoter driving TSP-1 transcription in vascular smooth muscle cells.
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An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpcell.00068.2016" target="_blank" rel="noreferrer noopener">10.1152/ajpcell.00068.2016</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*cAMP response element-binding protein
*interferon regulatory factor-1
*leptin
*thrombospondin-1
*Transcription
*vascular smooth muscle cells
2016
American journal of physiology. Cell physiology
Binding Sites/genetics
Cells
Chromatin Immunoprecipitation/methods
Cultured
Cyclic AMP Response Element-Binding Protein/*metabolism
Department of Integrative Medical Sciences
Ganguly Rituparna
Gene Expression Regulation/genetics
Genetic/genetics
Humans
Interferon Regulatory Factor-1/*metabolism
Leptin/*metabolism
Muscle
Mutagenesis
Myocytes
NEOMED College of Medicine
Promoter Regions
Raman Priya
Response Elements/genetics
Sahu Soumyadip
Site-Directed/methods
Smooth
Smooth Muscle/*metabolism
Thrombospondin 1/*genetics/*metabolism
Transcription
Transcriptional Activation/genetics
Transfection/methods
Up-Regulation/genetics
Vascular/*metabolism
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.18632/oncotarget.8405" target="_blank" rel="noreferrer noopener">http://doi.org/10.18632/oncotarget.8405</a>
Pages
25849–25861
Issue
18
Volume
7
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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TRPV4 channels regulate tumor angiogenesis via modulation of Rho/Rho kinase pathway.
Publisher
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Oncotarget
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-05
Subject
The topic of the resource
Animals; Mice; TRPV4; endothelial cell; Cell Movement/physiology; Endothelial Cells/metabolism/pathology; mechanotransduction; rho-Associated Kinases/*metabolism; Rho/Rho kinase; TRPV Cation Channels/*metabolism; tumor angiogenesis; Carcinoma; Inbred C57BL; Knockout; Neovascularization; Lewis Lung/metabolism/*pathology; Pathologic/*metabolism/pathology
Creator
An entity primarily responsible for making the resource
Thoppil Roslin J; Cappelli Holly C; Adapala Ravi K; Kanugula Anantha K; Paruchuri Sailaja; Thodeti Charles K
Description
An account of the resource
Targeting angiogenesis is considered a promising therapy for cancer. Besides curtailing soluble factor mediated tumor angiogenesis, understanding the unexplored regulation of angiogenesis by mechanical cues may lead to the identification of novel therapeutic targets. We have recently shown that expression and activity of mechanosensitive ion channel transient receptor potential vanilloid 4 (TRPV4) is suppressed in tumor endothelial cells and restoring TRPV4 expression or activation induces vascular normalization and improves cancer therapy. However, the molecular mechanism(s) by which TRPV4 modulates angiogenesis are still in their infancy. To explore how TRPV4 regulates angiogenesis, we have employed TRPV4 null endothelial cells (TRPV4KO EC) and TRPV4KO mice. We found that absence of TRPV4 (TRPV4KO EC) resulted in a significant increase in proliferation, migration, and abnormal tube formation in vitro when compared to WT EC. Concomitantly, sprouting angiogenesis ex vivo and vascular growth in vivo was enhanced in TRPV4KO mice. Mechanistically, we observed that loss of TRPV4 leads to a significant increase in basal Rho activity in TRPV4KO EC that corresponded to their aberrant mechanosensitivity on varying stiffness ECM gels. Importantly, pharmacological inhibition of the Rho/Rho kinase pathway by Y-27632 normalized abnormal mechanosensitivity and angiogenesis exhibited by TRPV4KO EC in vitro. Finally, Y-27632 treatment increased pericyte coverage and in conjunction with Cisplatin, significantly reduced tumor growth in TRPV4KO mice. Taken together, these data suggest that TRPV4 regulates angiogenesis endogenously via modulation of EC mechanosensitivity through the Rho/Rho kinase pathway and can serve as a potential therapeutic target for cancer therapy.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.18632/oncotarget.8405" target="_blank" rel="noreferrer noopener">10.18632/oncotarget.8405</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2016
Adapala Ravi K
Animals
Cappelli Holly C
Carcinoma
Cell Movement/physiology
Department of Integrative Medical Sciences
endothelial cell
Endothelial Cells/metabolism/pathology
Inbred C57BL
Kanugula Anantha K
Knockout
Lewis Lung/metabolism/*pathology
Mechanotransduction
Mice
NEOMED College of Medicine
Neovascularization
Oncotarget
Paruchuri Sailaja
Pathologic/*metabolism/pathology
rho-Associated Kinases/*metabolism
Rho/Rho kinase
Thodeti Charles K
Thoppil Roslin J
TRPV Cation Channels/*metabolism
TRPV4
tumor angiogenesis
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1038/srep24277" target="_blank" rel="noreferrer noopener">http://doi.org/10.1038/srep24277</a>
Pages
24277–24277
Volume
6
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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Carboxylesterase 1 Is Regulated by Hepatocyte Nuclear Factor 4alpha and Protects Against Alcohol- and MCD diet-induced Liver Injury.
Publisher
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Scientific reports
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-04
Subject
The topic of the resource
Alcoholic/*pathology; Alcohols/*toxicity; Animals; Carboxylic Ester Hydrolases/*metabolism; Chemical and Drug Induced Liver Injury/*pathology; Diet/*adverse effects; Fatty Liver; Gene Expression Regulation; Genetic; Hepatocyte Nuclear Factor 4/*metabolism; Hepatocytes/metabolism; Humans; Inbred C57BL; Knockout; Mice; Promoter Regions; Protein Binding
Creator
An entity primarily responsible for making the resource
Xu Jiesi; Xu Yang; Li Yuanyuan; Jadhav Kavita; You Min; Yin Liya; Zhang Yanqiao
Description
An account of the resource
The liver is a major organ that controls hepatic and systemic homeostasis. Dysregulation of liver metabolism may cause liver injury. Previous studies have demonstrated that carboxylesterase 1 (CES1) regulates hepatic triglyceride metabolism and protects against liver steatosis. In the present study, we investigated whether CES1 played a role in the development of alcoholic liver disease (ALD) and methionine and choline-deficient (MCD) diet-induced liver injury. Both hepatocyte nuclear factor 4alpha (HNF4alpha) and CES1 were markedly reduced in patients with alcoholic steatohepatitis. Alcohol repressed both HNF4alpha and CES1 expression in primary hepatocytes. HNF4alpha regulated CES1 expression by directly binding to the proximal promoter of CES1. Global inactivation of CES1 aggravated alcohol- or MCD diet-induced liver inflammation and liver injury, likely as a result of increased production of acetaldehyde and reactive oxygen species and mitochondrial dysfunctions. Knockdown of hepatic CES1 exacerbated ethanol-induced steatohepatitis. These data indicate that CES1 plays a crucial role in protection against alcohol- or MCD diet-induced liver injury.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1038/srep24277" target="_blank" rel="noreferrer noopener">10.1038/srep24277</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2016
Alcoholic/*pathology
Alcohols/*toxicity
Animals
Carboxylic Ester Hydrolases/*metabolism
Chemical and Drug Induced Liver Injury/*pathology
Department of Integrative Medical Sciences
Department of Pharmaceutical Sciences
Diet/*adverse effects
Fatty Liver
Gene Expression Regulation
Genetic
Hepatocyte Nuclear Factor 4/*metabolism
Hepatocytes/metabolism
Humans
Inbred C57BL
Jadhav Kavita
Knockout
Li Yuanyuan
Mice
NEOMED College of Medicine
NEOMED College of Pharmacy
Promoter Regions
Protein Binding
Scientific reports
Xu Jiesi
Xu Yang
Yin Liya
You Min
Zhang Yanqiao
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1002/hep.28712" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/hep.28712</a>
Pages
1072–1085
Issue
4
Volume
64
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Farnesoid X receptor activation increases reverse cholesterol transport by modulating bile acid composition and cholesterol absorption in mice.
Publisher
An entity responsible for making the resource available
Hepatology (Baltimore, Md.)
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-10
Subject
The topic of the resource
*Intestinal Absorption; Animals; Bile Acids and Salts/*chemistry; Biological Transport; Cholesterol/*metabolism; Cytoplasmic and Nuclear/*physiology; Inbred C57BL; Mice; Receptors
Creator
An entity primarily responsible for making the resource
Xu Yang; Li Fei; Zalzala Munaf; Xu Jiesi; Gonzalez Frank J; Adorini Luciano; Lee Yoon-Kwang; Yin Liya; Zhang Yanqiao
Description
An account of the resource
UNLABELLED: Activation of farnesoid X receptor (FXR) markedly attenuates development of atherosclerosis in animal models. However, the underlying mechanism is not well elucidated. Here, we show that the FXR agonist, obeticholic acid (OCA), increases fecal cholesterol excretion and macrophage reverse cholesterol transport (RCT) dependent on activation of hepatic FXR. OCA does not increase biliary cholesterol secretion, but inhibits intestinal cholesterol absorption. OCA markedly inhibits hepatic cholesterol 7alpha-hydroxylase (Cyp7a1) and sterol 12alpha-hydroxylase (Cyp8b1) partly through inducing small heterodimer partner, leading to reduced bile acid pool size and altered bile acid composition, with the alpha/beta-muricholic acid proportion in bile increased by 2.6-fold and taurocholic acid (TCA) level reduced by 71%. Overexpression of Cyp8b1 or concurrent overexpression of Cyp7a1 and Cyp8b1 normalizes TCA level, bile acid composition, and intestinal cholesterol absorption. CONCLUSION: Activation of FXR inhibits intestinal cholesterol absorption by modulation of bile acid pool size and composition, thus leading to increased RCT. Targeting hepatic FXR and/or bile acids may be useful for boosting RCT and preventing the development of atherosclerosis. (Hepatology 2016;64:1072-1085).
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1002/hep.28712" target="_blank" rel="noreferrer noopener">10.1002/hep.28712</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Intestinal Absorption
2016
Adorini Luciano
Animals
Bile Acids and Salts/*chemistry
Biological Transport
Cholesterol/*metabolism
Cytoplasmic and Nuclear/*physiology
Department of Integrative Medical Sciences
Gonzalez Frank J
Hepatology (Baltimore, Md.)
Inbred C57BL
Lee Yoon-Kwang
Li Fei
Mice
NEOMED College of Medicine
Receptors
Xu Jiesi
Xu Yang
Yin Liya
Zalzala Munaf
Zhang Yanqiao