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Liver fibrosis is mediated by hepatic stellate cells (HSCs), which respond to a variety of cytokine and growth factors to moderate the response to injury and create extracellular matrix at the site of injury. G-protein coupled receptor (GPCR)-mediated signaling, via endothelin-1 (ET-1) and angiotensin II (AngII), increases HSC contraction, migration and fibrogenesis. Regulator of G-protein signaling-5 (RGS5), an inhibitor of vasoactive GPCR agonists, functions to control GPCR-mediated contraction and hypertrophy in pericytes and smooth muscle cells (SMCs). Therefore we hypothesized that RGS5 controls GPCR signaling in activated HSCs in the context of liver injury. In this study, we localize RGS5 to the HSCs and demonstrate that  Rgs5  expression is regulated during carbon tetrachloride (CCl 4 )-induced acute and chronic liver injury in  Rgs5 LacZ/LacZ   reporter mice. Furthermore, CCl 4  treated RGS5-null mice develop increased hepatocyte damage and fibrosis in response to CCl 4  and have increased expression of markers of HSC activation. Knockdown of  Rgs5  enhances ET-1-mediated signaling in HSCs  in vitro . Taken together, we demonstrate that RGS5 is a critical regulator of GPCR signaling in HSCs and regulates HSC activation and fibrogenesis in liver injury.

Regulator of G-Protein Signaling-5 Is a Marker of Hepatic Stellate Cells and Expression Mediates Response to Liver Injury