1
40
5
-
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/10.1124/dmd.108.025155" target="_blank" rel="noreferrer noopener">http://doi.org/10.1124/dmd.108.025155</a>
Pages
469–478
Issue
3
Volume
37
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
Mechanism of vitamin D receptor inhibition of cholesterol 7alpha-hydroxylase gene transcription in human hepatocytes.
Publisher
An entity responsible for making the resource available
Drug metabolism and disposition: the biological fate of chemicals
Date
A point or period of time associated with an event in the lifecycle of the resource
2009
2009-03
Subject
The topic of the resource
Base Sequence; Calcitriol/drug effects/genetics/*physiology; Cell Line; Cells; Cholesterol 7-alpha-Hydroxylase/*genetics; Cultured; DNA Primers; Electrophoretic Mobility Shift Assay; Gene Knockdown Techniques; Genetic/*physiology; Hepatocytes/*drug effects/enzymology; Humans; Immunoprecipitation; Lithocholic Acid/pharmacology; Messenger/genetics; Polymerase Chain Reaction; Receptors; RNA; Small Interfering; Transcription; Tumor; Two-Hybrid System Techniques
Creator
An entity primarily responsible for making the resource
Han Shuxin; Chiang John Y L
Description
An account of the resource
Lithocholic acid (LCA) is a potent endogenous vitamin D receptor (VDR) ligand. In cholestasis, LCA levels increase in the liver and intestine. The objective of this study is to test the hypothesis that VDR plays a role in inhibiting cholesterol 7alpha-hydroxylase (CYP7A1) gene expression and bile acid synthesis in human hepatocytes. Immunoblot analysis has detected VDR proteins in the nucleus of the human hepatoma cell line HepG2 and human primary hepatocytes. 1alpha, 25-Dihydroxy-vitamin D(3) or LCA acetate-activated VDR inhibited CYP7A1 mRNA expression and bile acid synthesis, whereas small interfering RNA to VDR completely abrogated VDR inhibition of CYP7A1 mRNA expression in HepG2 cells. Electrophoretic mobility shift assay and mutagenesis analyses have identified the negative VDR response elements that bind VDR/retinoid X receptor alpha in the human CYP7A1 promoter. Mammalian two-hybrid, coimmunoprecipitation, glutathione
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1124/dmd.108.025155" target="_blank" rel="noreferrer noopener">10.1124/dmd.108.025155</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).
2009
Base Sequence
Calcitriol/drug effects/genetics/*physiology
Cell Line
Cells
Chiang John Y L
Cholesterol 7-alpha-Hydroxylase/*genetics
Cultured
Department of Integrative Medical Sciences
DNA Primers
Drug metabolism and disposition: the biological fate of chemicals
Electrophoretic Mobility Shift Assay
Gene Knockdown Techniques
Genetic/*physiology
Han Shuxin
Hepatocytes/*drug effects/enzymology
Humans
Immunoprecipitation
Lithocholic Acid/pharmacology
Messenger/genetics
NEOMED College of Medicine
Polymerase Chain Reaction
Receptors
RNA
Small Interfering
Transcription
Tumor
Two-Hybrid System Techniques
-
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.yjmcc.2012.10.016" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.yjmcc.2012.10.016</a>
Pages
45–52
Volume
54
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
TRPV4 channels mediate cardiac fibroblast differentiation by integrating mechanical and soluble signals.
Publisher
An entity responsible for making the resource available
Journal of molecular and cellular cardiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2013
2013-01
Subject
The topic of the resource
*Calcium Signaling; *Cell Differentiation; *Mechanotransduction; Animals; Cellular; Extracellular Matrix/metabolism/physiology; Fibroblasts/*physiology; Gene Knockdown Techniques; Male; Monoterpenes/pharmacology; Myocardium/cytology; Myofibroblasts/metabolism; Rats; RNA; Small Interfering/genetics; Sprague-Dawley; Transforming Growth Factor beta1/physiology; TRPM Cation Channels/antagonists & inhibitors/metabolism; TRPV Cation Channels/genetics/*metabolism
Creator
An entity primarily responsible for making the resource
Adapala Ravi K; Thoppil Roslin J; Luther Daniel J; Paruchuri Sailaja; Meszaros J Gary; Chilian William M; Thodeti Charles K
Description
An account of the resource
The phenotypic switch underlying the differentiation of cardiac fibroblasts into hypersecretory myofibroblasts is critical for cardiac remodeling following myocardial infarction. Myofibroblasts facilitate wound repair in the myocardium by secreting and organizing extracellular matrix (ECM) during the wound healing process. However, the molecular mechanisms involved in myofibroblast differentiation are not well known. TGF-beta has been shown to promote differentiation and this, combined with the robust mechanical environment in the heart, lead us to hypothesize that the mechanotransduction and TGF-beta signaling pathways play active roles in the differentiation of cardiac fibroblasts to myofibroblasts. Here, we show that the mechanosensitve ion channel TRPV4 is required for TGF-beta1-induced differentiation of cardiac fibroblasts into myofibroblasts. We found that the TRPV4-specific antagonist AB159908 and siRNA knockdown of TRPV4 significantly inhibited TGFbeta1-induced differentiation as measured by incorporation of alpha-SMA into stress fibers. Further, we found that
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.yjmcc.2012.10.016" target="_blank" rel="noreferrer noopener">10.1016/j.yjmcc.2012.10.016</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).
*Calcium Signaling
*Cell Differentiation
*Mechanotransduction
2013
Adapala Ravi K
Animals
Cellular
Chilian William M
Department of Integrative Medical Sciences
Extracellular Matrix/metabolism/physiology
Fibroblasts/*physiology
Gene Knockdown Techniques
Journal of molecular and cellular cardiology
Luther Daniel J
Male
Meszaros J Gary
Monoterpenes/pharmacology
Myocardium/cytology
Myofibroblasts/metabolism
NEOMED College of Medicine
Paruchuri Sailaja
Rats
RNA
Small Interfering/genetics
Sprague-Dawley
Thodeti Charles K
Thoppil Roslin J
Transforming Growth Factor beta1/physiology
TRPM Cation Channels/antagonists & inhibitors/metabolism
TRPV Cation Channels/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/10.1016/j.bbalip.2009.05.004" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.bbalip.2009.05.004</a>
Pages
991–996
Issue
10
Volume
1791
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
Forkhead box transcription factor O1 inhibits cholesterol 7alpha-hydroxylase in human hepatocytes and in high fat diet-fed mice.
Publisher
An entity responsible for making the resource available
Biochimica et biophysica acta
Date
A point or period of time associated with an event in the lifecycle of the resource
2009
2009-10
Subject
The topic of the resource
Adenoviridae/genetics; Animals; Bile Acids and Salts/biosynthesis; Cell Line; Cell Nucleus/drug effects/metabolism; Cholesterol 7-alpha-Hydroxylase/*antagonists & inhibitors/genetics/metabolism; Dietary Fats/*administration & dosage/*pharmacology; Down-Regulation/drug effects; Enzymologic/drug effects; Feeding Behavior/*drug effects; Forkhead Box Protein O1; Forkhead Transcription Factors/genetics/*metabolism; Gene Expression Regulation; Gene Knockdown Techniques; Gene Transfer Techniques; Hepatocytes/drug effects/*enzymology; Humans; Inbred C57BL; Insulin Resistance; Insulin/metabolism; Male; Messenger/genetics/metabolism; Mice; RNA; RNA Interference/drug effects; Tumor
Creator
An entity primarily responsible for making the resource
Li Tiangang; Ma Huiyan; Park Young Joo; Lee Yoon-Kwang; Strom Stephen; Moore David D; Chiang John Y L
Description
An account of the resource
The conversion of cholesterol to bile acids is the major pathway for cholesterol catabolism. Bile acids are metabolic regulators of triglycerides and glucose metabolism in the liver. This study investigated the roles of FoxO1 in the regulation of cholesterol 7alpha-hydroxylase (CYP7A1) gene expression in primary human hepatocytes. Adenovirus-mediated expression of a phosphorylation defective and constitutively active form of FoxO1 (FoxO1-ADA) inhibited CYP7A1 mRNA expression and bile acid synthesis, while siRNA knockdown of FoxO1 resulted in a approximately 6-fold induction of CYP7A1 mRNA in human hepatocytes. Insulin caused rapid exclusion of FoxO1 from the nucleus and resulted in the induction of CYP7A1 mRNA expression, which was blocked by FoxO1-ADA. In high fat diet-fed mice, CYP7A1 mRNA expression was repressed and inversely correlated to increase hepatic FoxO1 mRNA expression and FoxO1 nuclear retention. In conclusion, our current study provides direct evidence that FoxO1 is a strong repressor of CYP7A1 gene expression and bile acid synthesis. Impaired regulation of FoxO1 may cause down-regulation of CYP7A1 gene expression and contribute to dyslipidemia in insulin resistance.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.bbalip.2009.05.004" target="_blank" rel="noreferrer noopener">10.1016/j.bbalip.2009.05.004</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).
2009
Adenoviridae/genetics
Animals
Bile Acids and Salts/biosynthesis
Biochimica et biophysica acta
Cell Line
Cell Nucleus/drug effects/metabolism
Chiang John Y L
Cholesterol 7-alpha-Hydroxylase/*antagonists & inhibitors/genetics/metabolism
Department of Integrative Medical Sciences
Dietary Fats/*administration & dosage/*pharmacology
Down-Regulation/drug effects
Enzymologic/drug effects
Feeding Behavior/*drug effects
Forkhead Box Protein O1
Forkhead Transcription Factors/genetics/*metabolism
Gene Expression Regulation
Gene Knockdown Techniques
Gene Transfer Techniques
Hepatocytes/drug effects/*enzymology
Humans
Inbred C57BL
Insulin Resistance
Insulin/metabolism
Lee Yoon-Kwang
Li Tiangang
Ma Huiyan
Male
Messenger/genetics/metabolism
Mice
Moore David D
NEOMED College of Medicine
Park Young Joo
RNA
RNA Interference/drug effects
Strom Stephen
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/10.1002/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
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).
*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/10.1002/art.39173" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/art.39173</a>
Pages
2117–2128
Issue
8
Volume
67
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
MicroRNA-9 promotion of interleukin-6 expression by inhibiting monocyte chemoattractant protein-induced protein 1 expression in interleukin-1beta-stimulated human chondrocytes.
Publisher
An entity responsible for making the resource available
Arthritis & rheumatology (Hoboken, N.J.)
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
2015-05
Subject
The topic of the resource
Academic Medical Centers; Aged; Articular/drug effects/*metabolism; Cartilage; Cells; Chondrocytes – Physiology; Chondrocytes/drug effects/*metabolism; Cultured; Enzyme-Linked Immunosorbent Assay; Funding Source; Gene Knockdown Techniques; Hip/*genetics/metabolism; Human; Humans; Immunoblotting – Utilization; Immunoprecipitation; Interleukin-1beta/pharmacology; Interleukin-6/*genetics/metabolism; Interleukins – Physiology; Messenger/drug effects/*metabolism; MicroRNAs/drug effects/*genetics/metabolism; Middle Aged; Ohio; Osteoarthritis; Osteoarthritis – Complications; Osteoarthritis – Physiopathology; Reverse Transcriptase Polymerase Chain Reaction; Ribonucleases/drug effects/*genetics/metabolism; RNA; T-Tests; Transcription Factors/drug effects/*genetics/metabolism
Creator
An entity primarily responsible for making the resource
Makki Mohammad S; Haseeb Abdul; Haqqi Tariq M
Description
An account of the resource
OBJECTIVE: Enhanced expression of interleukin-6 (IL-6) plays an important role in the pathogenesis of osteoarthritis (OA). Monocyte chemoattractant protein-induced protein 1 (MCPIP-1) is a novel posttranscriptional regulator of IL-6 expression and is targeted by microRNA-9 (miR-9). We investigated the expression of MCPIP-1 in OA cartilage and explored whether targeting of MCPIP-1 by miR-9 contributes to enhanced IL-6 expression in OA. METHODS: Gene and protein expression in
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1002/art.39173" target="_blank" rel="noreferrer noopener">10.1002/art.39173</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).
2015
Academic Medical Centers
Aged
Arthritis & rheumatology (Hoboken, N.J.)
Articular/drug effects/*metabolism
Cartilage
Cells
Chondrocytes – Physiology
Chondrocytes/drug effects/*metabolism
Cultured
Department of Anatomy & Neurobiology
Enzyme-Linked Immunosorbent Assay
Funding Source
Gene Knockdown Techniques
Haqqi Tariq M
Haseeb Abdul
Hip/*genetics/metabolism
Human
Humans
Immunoblotting – Utilization
Immunoprecipitation
Interleukin-1beta/pharmacology
Interleukin-6/*genetics/metabolism
Interleukins – Physiology
Makki Mohammad S
Messenger/drug effects/*metabolism
MicroRNAs/drug effects/*genetics/metabolism
Middle Aged
NEOMED College of Medicine
Ohio
Osteoarthritis
Osteoarthritis – Complications
Osteoarthritis – Physiopathology
Reverse Transcriptase Polymerase Chain Reaction
Ribonucleases/drug effects/*genetics/metabolism
RNA
T-Tests
Transcription Factors/drug effects/*genetics/metabolism