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Abstract
Cardiac fibrosis is defined as an abnormal accumulation of excessive extracellular matrix proteins, especially collagens, in the myocardium, which characterizes morphological feature of the structural myocardial remodeling that occurs in several cardiac diseases. Transforming growth factor- (TGF-) is a major contributor to fibrogenic responses, modulating fibroblast activation and promoting extracellular matrix deposition by up-regulating collagen and fibronectin synthesis and by decreasing matrix degradation through inhibition of activities of matrix metalloproteinases (MMPs). The present study was designed to investigate whether response gene to complement 32 (RGC32) is involved in the transformation of fibroblasts to myofibroblasts and whether RGC32 depletion or overexpression alters the expression of smooth muscle -actin (-SMA), an indicator of myofibroblasts, and ECM proteins. Our results suggest that RGC32 is a TGF- downstream target mediating the myofibroblast transition in the primary mouse cardiac fibroblasts (mCFs). RGC32 depletion attenuates while overexpression enhances the expression of -SMA and collagen I.