Endothelin-1 stimulates resistin gene expression

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Title:	Endothelin-1 stimulates resistin gene expression
Authors:	高永旭;Tang, Ya-Chu;Liu, Chi-Wei;Chang, Hsin-Huei;Juan, Chi-Chang;Kuo, Yow-Chii;Kao, Chung-Cheng;Huang, Yao-Ming;Kao, Yung-Hsi
Contributors:	生醫理工學院生命科學系
Keywords:	1-Phosphatidylinositol 3-kinase;3T3-L1 Cells;Actinomycin;Adipocytes;Adipogenesis;Adipose tissue;Adipose Tissue - metabolism;AKT protein;Androstadienes - chemistry;Animals;Anthracenes - chemistry;Butadienes - chemistry;c-Jun protein;Carbonyl compounds;Carbonyls;Chromones - chemistry;Dactinomycin - metabolism;Endothelin 1;Endothelin-1 - metabolism;Extracellular signal-regulated kinase;Flavonoids - chemistry;Gene expression;Gene Expression Profiling;Gene Expression Regulation;Hormones;Insulin resistance;Janus kinase;Janus kinase 2;JNK protein;Kinases;Male;MAP Kinase Kinase 4 - metabolism;Mice;Mice, Inbred C57BL;Morpholines - chemistry;Nitriles - chemistry;Norleucine;Oligopeptides - chemistry;Phosphorylation;Piperidines - chemistry;Proteins;Proto-Oncogene Proteins c-akt - metabolism;Receptors;Resistin - metabolism;Signal Transduction;Stat3 protein;STAT3 Transcription Factor - metabolism;Transcription factors;Tryptophan;Tyrphostins - chemistry;Wortmannin
Date:	2014-03-01
Issue Date:	2026-04-23 11:12:31 (UTC+8)
Publisher:	Endocrine Society;United States: Oxford University Press
Abstract:	摘要： Resistin and endothelin (ET)-1 have been reported to inhibit adipogenesis and regulate adipocyte insulin resistance, respectively. Although both hormones interact with each other, the exact signaling pathway of ET-1 to act on resistin gene expression is still unknown. Using 3T3-L1 adipocytes, we investigated the signaling pathways involved in ET-1-stimulated resistin gene expression. The up-regulation of resistin mRNA expression by ET-1 depends on concentration and timing. The concentration of ET-1 that increased resistin mRNA levels by 100%–250% was approximately 100 nM for a range of 0.25–12 hours of treatment. Treatment with actinomycin D blocked ET-1-increased resistin mRNA levels, suggesting that the effect of ET-1 requires new mRNA synthesis. Treatment with an inhibitor of the ET type-A receptor, such as N-[1-Formyl-N-[N-[(hexahydro-1H-azepin-1-yl)carbonyl]-L-leucyl]-D-tryptophyl]-D-tryptophan (BQ610), but not with the ET type-B receptor antagonist N-[(cis-2,6-Dimethyl-1-piperidinyl)carbonyl]-4-methyl-L-leucyl-1-(methoxycarbonyl)-D-tryptophyl-D-norleucine (BQ788), blocked ET-1, increased the levels of resistin mRNA, and phosphorylated levels of downstream signaling molecules, such as ERK1/2, c-Jun N-terminal kinases (JNKs), protein kinase B (AKT), and signal transducer and activator of transcription 3 (STAT3). Moreover, pretreatment of specific inhibitors of either ERK1/2 (1,4-diamino-2,3-dicyano-1,4-bis[2-aminophenylthio]butadiene [U0126] and 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one [PD98059], two inhibitors of MEK1), JNKs (SP600125), phosphatidylinositol 3-kinase/AKT (LY294002 and Wortmannin), or Janus kinase 2 (JAK2)/STAT3 ((E)-2-Cyano-3-(3,4-dihydrophenyl)-N-(phenylmethyl)-2-propenamide, AG490) prevented ET-1-increased levels of resistin mRNA and reduced the ET-1-stimulated phosphorylation of ERK1/2, JNKs, AKT, and STAT3, respectively. However, the p38 kinase antagonist 4-[5-(4-Fluorophenyl)-2-[4-(methylsulfonyl)phenyl]-1H-imidazol-4-yl]pyridine (SB203580) did not alter the effect of ET-1. These results imply that ET type-A receptor, ERK1/2, JNKs, AKT, and JAK2, but not ET type-B receptor or p38, are necessary for the ET-1 stimulation of resistin gene expression. In vivo observations that ET-1 increased resistin mRNA and protein levels in sc and epididymal adipose tissues support the in vitro findings. 其他題名： Endocrinology 出版者： United States: Oxford University Press 出版日期： 2014-03-01 出處： Endocrinology (Philadelphia), 2014-03, Vol.155 (3), p.854-864 版權： Copyright © 2014 by The Endocrine Society 2014 版權： Copyright © 2014 by The Endocrine Society 識別號： ISSN: 0013-7227 識別號： ISSN: 1945-7170 識別號： EISSN: 1945-7170 識別號： DOI: 10.1210/en.2013-1847 識別號： PMID: 24424064
Appears in Collections:	[Department of Life Science] journal & Dissertation

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