Protein kinase B/Akt activity is involved in renal TGF- (31 -driven epithelial-mesenchymal transition in vitro and in vivo

摘要

The molecular pathogenesis of diabetic nephropathy (DN), the leading cause of end-stage renal disease worldwide, is complex and not fully understood. Transforming growth factor-fi (TGF-pi) plays a critical role in many fibrotic disorders, including DN. In this study, we report protein kinase B (PKB/Akt) activation as a downstream event contributing to the pathophysiology of DN. We investigated the potential of PKB/Akt to mediate the profibrotic bioactions of TGF-J31 in kidney. Treatment of normal rat kidney epithelial cells (NRK52E) with TGF-pl resulted in activation of phosphatidylinositol 3-kinase (PI3K) and PKB/Akt as evidenced by increased Ser473 phosphorylation and GSK-3(3 phos-phorylation.