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Investigations into the Inhibitory Effects of Relaxin on Renal Myofibroblast Differentiation
Author(s) -
Samuel Chrishan S.,
Mookerjee Ishanee,
Halls Michelle L.,
Summers Roger J.,
Chew Elaine,
Bathgate Ross A. D.,
Tregear Geoffrey W.,
Hewitson Tim D.
Publication year - 2009
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2008.03823.x
Subject(s) - relaxin , myofibroblast , inhibitory postsynaptic potential , chemistry , microbiology and biotechnology , medicine , endocrinology , biology , receptor , fibrosis
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 α‐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‐β1 (TGF‐β1) 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‐β1 remain unknown. In this report, the inhibitory actions of relaxin on TGF‐β1‐induced renal myofibroblast differentiation are summarized to date, and the potential signaling pathways that are implicated in relaxin's inhibitory actions are discussed.