Abstract
Transforming growth factor beta 1 (TGF-β1) is associated with cardiac fibrosis through R-Smad signaling. c-Ski is known to inhibit the actions of activated R-Smad/Co-Smad dimers by forming a “disrupting bridge” that locks the entire DNA binding complex in an inactivated form. We investigated the effect of c-Ski overexpression on procollagen type I expression in primary rat myofibroblasts in vitro. Using a pMixie-EGFP/c-Ski retroviral construct to overdrive exogenous c-Ski expression in P1 cells, procollagen type I expression was noted in the presence or absence of TGF-β1 (10 ng/ml, 30 min) with immunofluorescence and Western analysis.
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