1
40
14
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<a href="http://doi.org/10.1016/j.molmet.2021.101244" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.molmet.2021.101244</a>
Pages
3-11
ISSN
2212-8778
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Title
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Hepatocyte miR-34a is a key regulator in the development and progression of non-alcoholic fatty liver disease.
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Molecular Metabolism
Date
A point or period of time associated with an event in the lifecycle of the resource
2021
2021-04-27
Subject
The topic of the resource
miR-34a; NAFLD; Lipogenesis; bile acids; Bile acids; lipid absorption; lipogenesis; Lipid absorption
Creator
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Xu Y; Zhu Y; Hu S; Pan X; Bawa FC; Wang HH; Wang DQ; Yin L; Zhang Y
Description
An account of the resource
Objectives: Hepatic miR-34a expression is elevated in diet-induced or genetically obese mice, and patients with non-alcoholic steatohepatitis (NASH), yet the role of hepatocyte miR-34a in the progression of non-alcoholic fatty liver disease (NAFLD) from non-alcoholic fatty liver (NAFL) to NASH remains to be elucidated.; Methods: Mice over-expressing or deficient in hepatocyte miR-34a and their control mice were fed a diet enriched in fats, cholesterol and fructose (HFCF) to induce NASH. C57BL/6 mice with NASH were treated with an miR-34a inhibitor or a scramble control oligo. The effect of miR-34a on the development, progression or reversal of NAFLD was determined.; Results: Hepatocyte-specific expression of miR-34a aggravated HFCF diet-induced NAFLD. In contrast, germline or adult-onset loss of hepatocyte miR-34a attenuated the development and progression of NAFLD. In addition, pharmacological inhibition of miR-34a reversed HFCF diet-induced steatohepatitis. Mechanistically, hepatocyte miR-34a regulated the development and progression of NAFLD by inducing lipid absorption, lipogenesis, inflammation and apoptosis, and inhibiting fatty acid oxidation.; Conclusions: Hepatocyte miR-34a is an important regulator in the development and progression of NAFLD. MiR-34a may be a useful target for treating NAFLD. (Copyright © 2021 The Author(s). Published by Elsevier GmbH.. All rights reserved.)
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<a href="http://doi.org/10.1016/j.molmet.2021.101244" target="_blank" rel="noreferrer noopener">10.1016/j.molmet.2021.101244</a>
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journalArticle
2021
Bawa FC
BILE acids
Department of Integrative Medical Sciences
Hu S
journalArticle
lipid absorption
Lipogenesis
May 2021 List
miR-34a
Molecular metabolism
NAFLD
NEOMED College of Medicine
NEOMED Postdoc Publications
NEOMED Student Publications
Pan X
Wang DQ
Wang HH
Xu Y
Yin L
Zhang Y
Zhu Y
-
Text
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<a href="http://doi.org/10.1007/s10456-021-09775-9" target="_blank" rel="noreferrer noopener">http://doi.org/10.1007/s10456-021-09775-9</a>
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ISSN
1573-7209 0969-6970
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Department of Integrative Medical Sciences
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Title
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Endothelial TRPV4 channels prevent tumor growth and metastasis via modulation of tumor angiogenesis and vascular integrity.
Publisher
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Angiogenesis
Date
A point or period of time associated with an event in the lifecycle of the resource
2021
2021-03-03
Subject
The topic of the resource
Endothelial cell; Metastasis; Transient receptor potential vanilloid 4; Tumor angiogenesis; Vascular endothelial growth factor receptor 2
Creator
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Kanugula AK; Adapala RK; Jamaiyar A; Lenkey N; Guarino BD; Liedtke W; Yin L; Paruchuri S; Thodeti CK
Description
An account of the resource
Transient receptor potential vanilloid 4 (TRPV4) is a ubiquitously expressed polymodally activated ion channel. TRPV4 has been implicated in tumor progression; however, the cell-specific role of TRPV4 in tumor growth, angiogenesis, and metastasis is unknown. Here, we generated endothelial-specific TRPV4 knockout (TRPV4(ECKO)) mice by crossing TRPV4(lox/lox) mice with Tie2-Cre mice. Tumor growth and metastasis were significantly increased in a syngeneic Lewis lung carcinoma tumor model of TRPV4(ECKO) mice compared to TRPV4(l)(ox/lox) mice. Multiphoton microscopy, dextran leakage, and immunohistochemical analysis revealed increased tumor angiogenesis and metastasis that were correlated with aberrant leaky vessels (increased width and reduced pericyte and VE-cadherin coverage). Mechanistically, increases in VEGFR2, p-ERK, and MMP-9 expression and DQ gelatinase activity were observed in the TRPV4(ECKO) mouse tumors. Our results demonstrated that endothelial TRPV4 is a critical modulator of vascular integrity and tumor angiogenesis and that deletion of TRPV4 promotes tumor angiogenesis, growth, and metastasis.
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<a href="http://doi.org/10.1007/s10456-021-09775-9" target="_blank" rel="noreferrer noopener">10.1007/s10456-021-09775-9</a>
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journalArticle
2021
Adapala RK
angiogenesis
Department of Integrative Medical Sciences
endothelial cell
Guarino BD
Jamaiyar A
journalArticle
Kanugula AK
Lenkey N
Liedtke W
March 2021 List
Metastasis
NEOMED College of Medicine
NEOMED Postdoc Publications
NEOMED Student Publications
Paruchuri S
Thodeti CK
Transient receptor potential vanilloid 4
tumor angiogenesis
Vascular endothelial growth factor receptor 2
Yin L
-
Text
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<a href="http://doi.org/" target="_blank" rel="noreferrer noopener">http://doi.org/</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).
Pages
G166-G174
Issue
2
Volume
320
ISSN
1931857
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Title
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Hepatocyte-specific expression of human carboxylesterase 2 attenuates nonalcoholic steatohepatitis in mice.
Publisher
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American Journal Of Physiology: Gastrointestinal & Liver Physiology
Date
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2021
2021-02
Subject
The topic of the resource
steatohepatitis; LABORATORY mice; FATTY liver; lipotoxicity; CES2; fatty acid oxidation; lipolysis; FATTY acid oxidation; INSULIN sensitivity; STEROL regulatory element-binding proteins
Creator
An entity primarily responsible for making the resource
Xu Y;Pan X; Shuwei H;Zhu Y; Bawa FC;Li Y; Yin L; Zhang Y
Description
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Human carboxylesterase 2 (CES2) has triacylglycerol hydrolase (TGH) activities and plays an important role in lipolysis. In this study, we aim to determine the role of human CES2 in the progression or reversal of steatohepatitis in diet-induced or genetically obese mice. High-fat/high-cholesterol/high-fructose (HFCF) diet-fed C57BL/6 mice or db/db mice were intravenously injected with an adeno-associated virus expressing human CES2 under the control of an albumin promoter. Human CES2 protected against HFCF diet-induced nonalcoholic fatty liver disease (NAFLD) in C57BL/6J mice and reversed steatohepatitis in db/db mice. Human CES2 also improved glucose tolerance and insulin sensitivity. Mechanistically, human CES2 reduced hepatic triglyceride (T) and free fatty acid (FFA) levels by inducing lipolysis and fatty acid oxidation and inhibiting lipogenesis via suppression of sterol regulatory element-binding protein 1. Furthermore, human CES2 overexpression improved mitochondrial respiration and glycolytic function, and inhibited gluconeogenesis, lipid peroxidation, apoptosis, and inflammation. Our data suggest that hepatocyte-specific expression of human CES2 prevents and reverses steatohepatitis. Targeting hepatic CES2 may be an attractive strategy for treatment of NAFLD. NEW & NOTEWORTHY Human CES2 attenuates high-fat/cholesterol/fructose diet-induced steatohepatitis and reverses steatohepatitis in db/db mice. Mechanistically, human CES2 induces lipolysis, fatty acid and glucose oxidation, and inhibits hepatic glucose production, inflammation, lipid oxidation, and apoptosis. Our data suggest that human CES2 may be targeted for treatment of non-alcoholic steatohepatitis (NASH). [ABSTRACT FROM AUTHOR]
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<a href="http://doi.org/10.1152/ajpgi.00315.2020" target="_blank" rel="noreferrer noopener">10.1152/ajpgi.00315.2020</a>
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The file format, physical medium, or dimensions of the resource
journalArticle
2021
American Journal Of Physiology: Gastrointestinal & Liver Physiology
Bawa FC
CES2
Department of Integrative Medical Sciences
Fatty acid oxidation
Fatty Liver
insulin sensitivity
journalArticle
LABORATORY mice
Li Y
Lipolysis
lipotoxicity
March 2021 List
NEOMED College of Medicine
NEOMED Postdoc Publications
Pan X
Shuwei H
steatohepatitis
STEROL regulatory element-binding proteins
Xu Y
Yin L
Zhang Y
Zhu Y
-
Text
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<a href="http://doi.org/10.1038/s42255-020-00331-1" target="_blank" rel="noreferrer noopener">http://doi.org/10.1038/s42255-020-00331-1</a>
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Pages
59-74
Issue
1
Volume
3
ISSN
2522-5812
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Title
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Hepatocyte ATF3 protects against atherosclerosis by regulating HDL and bile acid metabolism.
Date
A point or period of time associated with an event in the lifecycle of the resource
2021
2021-01
Subject
The topic of the resource
atherosclerosis
Creator
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Xu Y;Li Y;Jadhav K;Pan X;Zhu Y;Hu S;Chen S;Chen L;Tang Y;Wang HH;Yang L;Wang DQ;Yin L;Zhang Y
Description
An account of the resource
Activating transcription factor (ATF)3 is known to have an anti-inflammatory function, yet the role of hepatic ATF3 in lipoprotein metabolism or atherosclerosis remains unknown. Here we show that overexpression of human ATF3 in hepatocytes reduces the development of atherosclerosis in Western-diet-fed Ldlr(-/-) or Apoe(-/-) mice, whereas hepatocyte-specific ablation of Atf3 has the opposite effect. We further show that hepatic ATF3 expression is inhibited by hydrocortisone. Mechanistically, hepatocyte ATF3 enhances high-density lipoprotein (HDL) uptake, inhibits intestinal fat and cholesterol absorption and promotes macrophage reverse cholesterol transport by inducing scavenger receptor group B type 1 (SR-BI) and repressing cholesterol 12α-hydroxylase (CYP8B1) in the liver through its interaction with p53 and hepatocyte nuclear factor 4α, respectively. Our data demonstrate that hepatocyte ATF3 is a key regulator of HDL and bile acid metabolism and atherosclerosis.
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<a href="http://doi.org/10.1038/s42255-020-00331-1" target="_blank" rel="noreferrer noopener">10.1038/s42255-020-00331-1</a>
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journalArticle
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Nature Metabolism
2021
Atherosclerosis
Chen L
Chen S
Department of Integrative Medical Sciences
February 2021 List
Hu S
Jadhav K
journalArticle
Li Y
Nature Metabolism
NEOMED College of Medicine
NEOMED College of Medicine Postdoc
NEOMED Postdoc Publications
Pan X
Tang Y
Wang DQ-H
Wang HH
Xu Y
Yang L
Yin L
Zhang Y
Zhu Y
-
Text
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<a href="http://doi.org/10.1152/ajpgi.00315.2020" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpgi.00315.2020</a>
ISSN
1522-1547 0193-1857
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January 2021 List
NEOMED College
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Department of Integrative Medical Sciences
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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
Hepatocyte-specific expression of human carboxylesterase 2 attenuates non-alcoholic steatohepatitis in 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
2020
2020-12-16
Subject
The topic of the resource
CES2; Fatty acid oxidation; Lipolysis; Lipotoxicity; Steatohepatitis
Creator
An entity primarily responsible for making the resource
Xu Y; Pan X; Hu S; Zhu Y; Cassim BF; Li Y; Yin L; Zhang Y
Description
An account of the resource
Human carboxylesterase 2 (CES2) has triacylglycerol hydrolase (TGH) activities and plays an important role in lipolysis. In this study, we aim to determine the role of human CES2 in the progression or reversal of steatohepatitis in diet-induced or genetically obese mice. High-fat/high-cholesterol/high-fructose (HFCF) diet-fed C57BL/6 mice or db/db mice were i.v. injected with an adeno-associated virus expressing human CES2 under the control of an albumin promoter. Human CES2 protected against HFCF diet-induced non-alcoholic fatty liver disease (NAFLD) in C57BL/6J mice and reversed steatohepatitis in db/db mice. Human CES2 also improved glucose tolerance and insulin sensitivity. Mechanistically, human CES2 reduced hepatic triglyceride and free fatty acid levels by inducing lipolysis and fatty acid oxidation and inhibiting lipogenesis via suppression of sterol regulatory element-binding protein 1. Furthermore, human CES2 overexpression improved mitochondrial respiration and glycolytic function, and inhibited gluconeogenesis, lipid peroxidation, apoptosis and inflammation. Our data suggest that hepatocyte-specific expression of human CES2 prevents and reverses steatohepatitis. Targeting hepatic CES2 may be an attractive strategy for treatment of NAFLD.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpgi.00315.2020" target="_blank" rel="noreferrer noopener">10.1152/ajpgi.00315.2020</a>
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journalArticle
2020
American Journal of Physiology-Gastrointestinal and Liver Physiology
Cassim BF
CES2
Department of Integrative Medical Sciences
Fatty acid oxidation
Hu S
January 2021 List
journalArticle
Li Y
Lipolysis
lipotoxicity
NEOMED College of Medicine
NEOMED College of Medicine Postdoc
NEOMED Postdoc Publications
Pan X
steatohepatitis
Xu Y
Yin L
Zhang Y
Zhu Y
-
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/10.1161/circ.142.suppl_3.17248" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/circ.142.suppl_3.17248</a>
Pages
A17248-A17248
Issue
Suppl 3
Volume
142
ISSN
0009-7322
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Abstract 17248: The role of microRNA-21 in regulating the coronary microcirculation in diabetes
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Circulation
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-11-17
Creator
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Juguilon C; Wang Z; Gadd J;Ohanyan VA; Anurag J; Molly E; Wang T; Kolz C; William MC; Yin L
Description
An account of the resource
Introduction: Coronary microvascular dysfunction is prevalent among diabetics and intersects with deficits in endothelial-dependent vasodilation. These deficits occur early in the progression of the disease, but the mechanisms remain incompletely understood. Nitric oxide (NO) is the major endothelial-dependent mediator of vasodilation in the healthy coronary circulation, but the mediator switches to hydrogen peroxide (H2O2) in coronary artery disease (CAD) patients. Diabetes is a risk factor for CAD, so we hypothesized that a similar switch would occur.Methods: Coronary arteries were isolated and endothelial-dependent vasodilation was assessed using myography. Quantitative polymerase chain reaction (qPCR) was performed for gene expression analysis and myocardial blood flow (MBF) was measured by contrast echocardiography.Results: Nitric oxide synthase inhibitor (L-NAME) inhibited vasodilation in wild type (WT) mice, but the H2O2 scavenger (PEG-catalase) had no effect. In contrast, vasodilation in diabetic mice was blunted by PEG-catalase, but not L-NAME. This suggests that the mediator of coronary vasodilation switched from NO to H2O2 in diabetes. Importantly, we found that microRNA-21 (miR-21) is upregulated in diabetes and the deficiency modulates the mediator switch from NO to H2O2 in diabetic mice.Conclusions: The switch in the mediator of coronary vasodilation from NO to H2O2 contributes to microvascular dysfunction in diabetes and miR-21 regulates this switch. Further genetic profiling will elucidate the pathways and mechanisms converging with miR-21 to regulate microvascular function in diabetes. This is the first mouse model that recapitulates the switch in mediator of coronary vasodilation from NO to H2O2 seen in CAD patients.
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<a href="http://doi.org/10.1161/circ.142.suppl_3.17248" target="_blank" rel="noreferrer noopener">10.1161/circ.142.suppl_3.17248</a>
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journalArticle
2020
Anurag J
Circulation
December 2020 List
Department of Integrative Medical Sciences
Gadd J
journalArticle
Juguilon C
Kolz C
Molly E
NEOMED College of Graduate Studies
NEOMED College of Medicine
NEOMED Student Publications
Ohanyan VA
Wang T
Wang Z
William MC
Yin L
-
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/10.1096/fasebj.2020.34.s1.09506" target="_blank" rel="noreferrer noopener">http://doi.org/10.1096/fasebj.2020.34.s1.09506</a>
Issue
1
Volume
34
ISSN
0892-6638
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Title
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Regulation of coronary collateral growth by microrna-21 in metabolic syndrome
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Faseb Journal
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-04
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Juguilon C;Richardson D;Gadd J;Enrick M;Jamaiyar A;Xu Y;Wang Z;Wang T;Kolz C;Chilian W;Yin L
Description
An account of the resource
Well‐developed coronary collaterals prove to be highly beneficial in salvaging ischemic myocardium, preserving cardiac function, and improving patient outcome post‐occlusion. However, this process of coronary collateral growth (CCG) is impaired in patients with metabolic syndrome. A complete understanding of the underlying mechanism, cell types, and genes contributing towards this impairment have yet to be elucidated. Therefore, uncovering more about the process may lead to potential therapeutics to induce CCG in metabolic syndrome. MicroRNA‐21 (miR‐21) is abundantly expressed in vascular and immune cells with numerous implications in cardiovascular disease including atherosclerosis, heart failure, and myocardial infarction. Furthermore, miR‐21 has been shown to regulate processes such as apoptosis, immune cell polarization, and endothelial progenitor proliferation. Additionally, miR‐21 dysregulation has been rooted in the diabetic population where lies a systemic inflammatory state. In this study, we investigated the role of miR‐21 in a mouse model of CCG. Our preliminary data suggested that down‐regulating miR‐21 rescues impaired CCG in a diet‐induced model of metabolic syndrome. Thus, we investigated the underlying mechanism and focused on the roles of miR‐21 in the maintenance of vascular homeostasis, function and inflammatory responses in metabolic syndrome. First, we studied whether miR‐21 regulates endothelial homeostasis by modulating the function and homing of bone marrow stem cells in metabolic syndrome. We analyzed endothelial progenitor cells (CD34+) in bone marrow and peripheral blood, along with endothelial proliferation in WT, miR‐21 knockout, and metabolic syndrome mice. Second, we studied whether miR‐21 regulates the inflammatory response in metabolic syndrome by characterizing bone marrow derived macrophages from WT and miR‐21 knockout animals along with mapping their influence on vascular cells. Third, we utilized a myeloid specific miR‐21 knockout to study its role during CCG in vivo. We found CCG to be blunted in these animals which suggests the importance of myeloid derived miR‐21 in healthy mice. Further studies will give us more insight on miR‐21 and its regulation of CCG in metabolic syndrome.
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<a href="http://doi.org/10.1096/fasebj.2020.34.s1.09506" target="_blank" rel="noreferrer noopener">10.1096/fasebj.2020.34.s1.09506</a>
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journalArticle
2020
Chilian W
Department of Integrative Medical Sciences
Enrick M
Faseb Journal
Gadd J
Jamaiyar A
journalArticle
Juguilon C
Kolz C
NEOMED College of Medicine
NEOMED College of Medicine Postdoc
NEOMED College of Medicine Student
NEOMED Postdoc Publications
NEOMED Student Publications
Richardson D
September 2020 List
Wang T
Wang Z
Xu Y
Yin L
-
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/10.1096/fasebj.2020.34.s1.09453" target="_blank" rel="noreferrer noopener">http://doi.org/10.1096/fasebj.2020.34.s1.09453</a>
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1
Volume
34
ISSN
0892-6638
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<a href="http://neomed.idm.oclc.org/login?url=http://doi.org/10.1096/fasebj.2020.34.s1.09453" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1096/fasebj.2020.34.s1.09453</a>
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September 2020 List
NEOMED College
NEOMED College of Medicine
NEOMED Department
NEOMED Postdoc Publications
NEOMED Student Publications
Department of Integrative Medical Sciences
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Title
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Sprouting angiogenesis contributes to coronary collateral growth induced by repetitive ischemia in adult mice
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Faseb Journal
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-04
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Jamaiyar A;Juguilon C;Richardson D;Gadd J;Wang T;Enrick M;Goodner R;Chilian W;Yin L
Description
An account of the resource
In the United States, coronary heart diseases (CHD) are the leading cause of mortality and morbidity. A well‐developed coronary collateral circulation ameliorates the consequences of CHD, reducing the incidence of sudden death and infarct sizes following coronary occlusion. Stimulation of coronary collateral growth (CCG) is also an alternative therapeutic approach to patients with intractable angina pectoris. The importance of CCG is undisputable, but the process and mechanism underlying CCG is unclear. We developed a mouse model of CCG induced by repetitive ischemia (RI) and validated CCG by contrast echocardiography to measure the coronary blood flow in the normal zone (NZ) and the collateral dependent zone (CZ). We also used Micro‐CT scans to reconstruct the coronary vasculature in 3D and quantify CCG. In this study, we crossed ROSA mT/mG double fluorescent reporter mice with cell type‐specific cre mice to investigate the roles that different cell‐types play at various stages of CCG. Mice were subjected to the RI protocol and their cardiac function and coronary blood flow was measured by echocardiography. Following sacrifice, hearts were fixed for immunostaining or imaging under confocal and multiphoton microscopy. In ROSA mT/mG floxed, Apln cre mouse hearts, large vessels (diameter of 20–50 μm) expressing GFP were identified in the collateral dependent zone in the early stage of RI, indicating that they originated from sprouting endothelial cells. At the end of RI, a complete network of these vessels was observed anastomosing with existing vasculature from the NZ. Immunostaining revealed an outer layer of smooth muscle cells in these vessels, suggesting the arteriogenesis or arterialization. Interestingly, in ROSA mT/mG floxed, Lyz2 cre mouse hearts, GFP expressing myeloid cells were observed in high numbers around newly formed large vessels, suggesting that immune cell recruitment occurs in the early stages of CCG. Our preliminary data show that coronary collaterals form in response to RI, are of microvascular origin and are associated with early recruitment of immune cells to the CZ. Our further study will focus on the process of CCG in greater detail at the molecular and cellular level, potentially leading toward a therapeutic application of induced CCG in patients of ischemic heart diseases.
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<a href="http://doi.org/10.1096/fasebj.2020.34.s1.09453" target="_blank" rel="noreferrer noopener">10.1096/fasebj.2020.34.s1.09453</a>
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journalArticle
2020
Chilian W
Department of Integrative Medical Sciences
Enrick M
Faseb Journal
Gadd J
Goodner R
Jamaiyar A
journalArticle
Juguilon C
NEOMED College of Medicine
NEOMED College of Medicine Postdoc
NEOMED College of Medicine Student
NEOMED Postdoc Publications
NEOMED Student Publications
Richardson D
September 2020 List
Wang T
Yin L
-
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/10.1096/fasebj.2020.34.s1.05328" target="_blank" rel="noreferrer noopener">http://doi.org/10.1096/fasebj.2020.34.s1.05328</a>
Issue
1
Volume
34
ISSN
0892-6638
Search for Full-text
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<a href="http://neomed.idm.oclc.org/login?url=http://doi.org/10.1096/fasebj.2020.34.s1.05328" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1096/fasebj.2020.34.s1.05328</a>
<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
Update Year & Number
September 2020 List
NEOMED College
NEOMED College of Medicine
NEOMED Department
NEOMED Student Publications
Department of Integrative Medical Sciences
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Is chemotherapy-induced cardiomyopathy caused by myocardial ischemia?
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Faseb Journal
Date
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2020
2020-04
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Davidian A;Mistry M;Pucci T;Kolz C;Shockling L;Enrick M;Yin L;Chilian W;Ohanyan V
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Over the last 50 years progress has been made in treating childhood and adult solid and hematological tumors. One commonly used chemotherapeutic agent is doxorubicin (DOX), an anthracycline antitumor antibiotic, which was discovered in early 1960s. Anthracycline (ANT) chemotherapy alone or in combination with other chemotherapeutic agents markedly improves the survival rate of cancer patients, particularly among children, where survival rates have more than doubled over 5 decades. However, the use of ANT chemotherapy is a double‐edged sword in that it can produce chemotherapy induced cardiac dysfunction (CRCD), which can cause death in 50% of the patients with who present with the cardiomyopathy. We hypothesized, that one of the causes for CRGD is a reduction in myocardial blood flow (MBF) that leads to cardiac myocyte hypoxia, producing small areas of ischemia and myocyte damage. We also hypothesize that increasing MBF by the coronary vasodilator chromonar prevents cardiomyocytes from hypoxic damage. To test these hypotheses, we treated mice genetically engineered to show cardiac myocyte fluorescence if the cells are hypoxic (hypoxia fate mapping [HFM]) with DOX for 6 weeks (group 1, N=8) and Dox + Chromonar for 6 weeks (group 2 N=8). Five weeks after treatment we started tamoxifen for 5 days to activate the HFM protocol. Tamoxifen induces Cre in cardiac myocytes and hypoxia activates a program that results in the expression of td‐tomato only in hypoxic cardiac myocytes. In tissue sections, hypoxic cardiac myocytes are visualized by fluorescence microscopy. Cardiac function was measured by ultrasound and MBF was measured with contrast echocardiography. Six weeks after DOX treatment many hypoxic myocytes were observed in the myocardium. Cardiac function was significantly decreased at the end of DOX treatment (% ejection fraction EF=39±3) compared to baseline (62±5.8%). Simultaneous administration of chromonar prevents the cardiomyocytes from hypoxic damage and prevents cardiac dysfunction development. %EF was 58±6 at the end of the chemotherapy. Chromonar also significantly increased MBF in group 2 mice compared to group 1 (P<0.05). Based on these data CRCD may be a type of ischemic heart disease where the treatment reduces MBF, which leads cardiomyocyte hypoxia, and causes progressive, accumulative cardiac injury. Moreover, increasing myocardial blood flow by chromonar prevents the cardiomyocytes from hypoxic damage and development of CRCD.
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<a href="http://doi.org/10.1096/fasebj.2020.34.s1.05328" target="_blank" rel="noreferrer noopener">10.1096/fasebj.2020.34.s1.05328</a>
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journalArticle
2020
Chilian W
Davidian A
Department of Integrative Medicine
Enrick M
Faseb Journal
journalArticle
Kolz C
Mistry M
NEOMED College of Medicine
NEOMED College of Medicine Student
NEOMED Student Publications
Ohanyan V
Pucci T
September 2020 List
Shockling L
Yin L
-
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.
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n/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).
Pages
1-1
Volume
31
Search for Full-text
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Lack Of Efficient Metabolism Adaption Caused Failure Of Regenerative Cell-based Therapy In A Rat Model Of Metabolic Syndrome
Publisher
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Faseb Journal
Date
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2017
2017-04
Subject
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Biochemistry & Molecular Biology; Cell Biology; Life Sciences & Biomedicine - Other; Topics
Creator
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Jamaiyar A; Wan W G; Janota D; Enrick M; Ohanyan V; Yin L; Chilian W
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n/a
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Journal Article or Conference Abstract Publication
2017
Biochemistry & Molecular Biology
Cell Biology
Chilian W
Enrick M
Faseb Journal
Jamaiyar A
Janota D
Journal Article or Conference Abstract Publication
Life Sciences & Biomedicine - Other
Ohanyan V
Topics
Wan W G
Yin L
-
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
n/a
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
1-1
Volume
29
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Manipulation Of Induced Pluripotent Stem Cell Differentiation To Endothelial Cells
Publisher
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Faseb Journal
Date
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2015
2015-04
Subject
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Biochemistry & Molecular Biology; Cell Biology; Life Sciences & Biomedicine - Other; Topics
Creator
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DiVincenzo L; Kolz C; Chilian W; Yin L
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n/a
Format
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Journal Article or Conference Abstract Publication
2015
Biochemistry & Molecular Biology
Cell Biology
Chilian W
DiVincenzo L
Faseb Journal
Kolz C
Life Sciences & Biomedicine - Other
Topics
Yin L
-
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.
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n/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).
Pages
2-2
Issue
21
Volume
122
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Title
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Kv 1.5 Channels Play A Critical Role in Coronary Metabolic Dilation
Publisher
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Circulation
Date
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2010
2010-11
Subject
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Cardiovascular System & Cardiology; Coronary circulation; Coronary microcirculation; Potassium channel
Creator
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Ohanyan V A; Bratz I N; Guarini G; Yin L; Chilian W M
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n/a
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Journal Article
2010
Bratz I N
Cardiovascular System & Cardiology
Chilian W M
Circulation
Coronary Circulation
Coronary microcirculation
Guarini G
Journal Article
Ohanyan V A
Potassium channel
Yin L
-
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
n/a
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
2-2
Volume
30
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
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Title
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Catecholamine Induced Takotsubo Cardiomyopathy: The role of coronary metabolic blood flow regulation in apical ballooning
Publisher
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Faseb Journal
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-04
Subject
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Biochemistry & Molecular Biology; Cell Biology; Life Sciences & Biomedicine - Other; Topics
Creator
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Ohanyan V; Yin L; Bardakjian R; Khayata M; Kolz C L; Enrick M; Schatmeyer B; Perera V; Janota D; Hakobyan T; Chilian W M
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n/a
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Journal Article
2016
Bardakjian R
Biochemistry & Molecular Biology
Cell Biology
Chilian W M
Enrick M
Faseb Journal
Hakobyan T
Janota D
Journal Article
Khayata M
Kolz C L
Life Sciences & Biomedicine - Other
Ohanyan V
Perera V
Schatmeyer B
Topics
Yin L
-
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.pharmthera.2017.02.032" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.pharmthera.2017.02.032</a>
Pages
28–34
Volume
175
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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The versatility and paradox of GDF 11.
Publisher
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Pharmacology & therapeutics
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-07
Subject
The topic of the resource
Aging; Aging/metabolism; Animals; Biomarker; Biomarkers/metabolism; BMP signaling; Bone Morphogenetic Proteins/*metabolism; Development; Embryonic Development; Erythropoiesis; Growth differentiation factor 11; Growth Differentiation Factors/*metabolism; Humans; Neurogenesis; Pancreas/growth & development/metabolism; Retina/growth & development/metabolism
Creator
An entity primarily responsible for making the resource
Jamaiyar A; Wan W; Janota D M; Enrick M K; Chilian W M; Yin L
Description
An account of the resource
In addition to its roles in embryonic development, Growth and Differentiation Factor 11 (GDF 11) has recently drawn much interest about its roles in other processes, such as aging. GDF 11 has been shown to play pivotal roles in the rescue of the proliferative and regenerative capabilities of skeletal muscle, neural stem cells and cardiomyocytes. We would be remiss not to point that some controversy exists regarding the role of GDF 11 in biological processes and whether it will serve as a therapeutic agent. The latest studies have shown that the level of circulating GDF 11 correlates with the outcomes of patients with cardiovascular diseases, cancer and uremia. Based on these studies, GDF 11 is a promising candidate to serve as a novel biomarker of diseases. This brief review gives a detailed and concise view of the regulation and functions of GDF 11 and its roles in development, neurogenesis and erythropoiesis as well as the prospect of using this protein as an indicator of cardiac health and aging.
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<a href="http://doi.org/10.1016/j.pharmthera.2017.02.032" target="_blank" rel="noreferrer noopener">10.1016/j.pharmthera.2017.02.032</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).
2017
Aging
Aging/metabolism
Animals
Biomarker
Biomarkers/metabolism
BMP signaling
Bone Morphogenetic Proteins/*metabolism
Chilian W M
Department of Integrative Medical Sciences
development
Embryonic Development
Enrick M K
Erythropoiesis
Growth differentiation factor 11
Growth Differentiation Factors/*metabolism
Humans
Jamaiyar A
Janota D M
NEOMED College of Medicine
Neurogenesis
Pancreas/growth & development/metabolism
Pharmacology & therapeutics
Retina/growth & development/metabolism
Wan W
Yin L