AIM: The shift from the differentiated contractile smooth muscle cell phenotype to a less differentiated, proliferative state and excessive extracellular matrix (ECM) production, both TGF-β regulated events, are key alterations in atherogenesis. Response Gene to Complement (RGC)-32 is a mediator of the TGF-β downstream effects. Our goal was to explore the role of RGC-32 in mediation of TGF-β induced differentiation and ECM production by human aortic smooth muscle cells (ASMC). 
METHODS: We examined the expression of RGC-32, alpha-smooth muscle actin (as a marker of ASMC differentiation), collagen type I to V and fibronectin (as ECM components) in human aortic atherosclerotic lesions by immunohistochemistry. The effect of RGC-32 on alpha-smooth muscle actin (α-SMA) expression in ASMC was studied by silencing RGC-32 expression, using transfection of RGC-32 siRNA in the presence of Lipofectamine 3000. The expression of α-SMA, collagens I and fibronectin were determined by real-time PCR and western blot.
RESULTS:  RGC-32 was found to be expressed by ASMC in the human atherosclerotic wall and its expression was observed to increase with the progression of atherosclerosis. We investigated the role of RGC-32 in TGF-β-induced α-SMA and ECM production in ASMC. In cultured ASMC α-SMA, collagen I and fibronectin were significantly induced at 18 h of stimulation with TGF-β. RGC-32 silencing in ASMC led to a significant reduction in TGF-β induced α-SMA (p<0.02), fibronectin (p<0.05) and collagen I (p<0.03) expression. 
CONCLUSIONS: Our data infers that RGC-32 is a vital player in TGF-β-mediated differentiation and ECM production by ASMC, rendering it an attractive target for therapeutic intervention in atherosclerosis.

02 - RESPONSE GENE TO COMPLEMENT-32 MEDIATES AORTIC SMOOTH MUSCLE CELLS DIFFERENTIATION IN HUMAN ATHEROSCLEROTIC LESIONS