Investigations into the Inhibitory Effects of Relaxin on Renal Myofibroblast Differentiation

被引：6

作者：

Samuel, Chrishan S. ^{[1
,2
]}

Mookerjee, Ishanee ^{[1
,2
]}

Halls, Michelle L. ^{[3
]}

Summers, Roger J. ^{[3
]}

Chew, Elaine ^{[1
,2
]}

Bathgate, Ross A. D. ^{[1
,2
]}

Tregear, Geoffrey W. ^{[1
,2
]}

Hewitson, Tim D. ^{[4
,5
]}

机构：

[1] Univ Melbourne, Howard Florey Inst, Parkville, Vic 3010, Australia

[2] Univ Melbourne, Dept Biochem & Mol Biol, Parkville, Vic 3010, Australia

[3] Monash Univ, Dept Pharmacol, Clayton, Vic 3168, Australia

[4] Univ Melbourne, Royal Melbourne Hosp, Dept Nephrol, Parkville, Vic, Australia

[5] Univ Melbourne, Royal Melbourne Hosp, Dept Med, Parkville, Vic, Australia

来源：

RELAXIN AND RELATED PEPTIDES: FIFTH INTERNATIONAL CONFERENCE | 2009年 / 1160卷

基金：

澳大利亚国家健康与医学研究理事会; 澳大利亚研究理事会; 英国医学研究理事会;

关键词：

relaxin; myofibroblast; tubulointerstitial fibrosis; transforming growth factor-beta 1; alpha-smooth muscle actin; cell signaling; MULTIPLE SIGNALING PATHWAYS; FAMILY PEPTIDE RECEPTORS; HUMAN MESANGIAL CELLS; HORMONE RELAXIN; FIBROBLAST FUNCTION; PREGNANCY HORMONE; THP-1; CELLS; MAP KINASE; KAPPA-B; ACTIVATION;

D O I：

10.1111/j.1749-6632.2008.03823.x

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Derived from fibroblasts, myofibroblasts are the principal cells that are responsible for the synthesis and reorganization of excess matrix in renal interstitial fibrosis. Recognized from their de novo expression of a-smooth muscle actin, myofibroblast differentiation and activity can be influenced by several factors, including a combination of growth factors and other soluble mediators, extracellular matrix components, and mechanical stress. Relaxin has previously been shown to inhibit renal myofibroblast differentiation in vitro, an effect partly mediated through its ability to interfere with the transforming growth factor-beta 1 (TGF-beta 1) pathway via inhibition of Smad2 phosphorylation and translocation. Furthermore, endogenous relaxin has been shown to protect the kidney from a myofibroblast-mediated model of injury in vivo. However, the pathways involved in the interaction between relaxin and TGF-beta 1 remain unknown. In this report, the inhibitory actions of relaxin on TGF-beta 1-induced renal myofibroblast differentiation are summarized to date, and the potential signaling pathways that are implicated in relaxin's inhibitory actions are discussed.

引用

页码：294 / 299

页数：6

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