PKC-β1 mediates glucose-induced akt activation and TGF-β1 upregulation in mesangial cells

Abstract

Accumulation of glomerular matrix is a hallmark of diabetic nephropathy. The serine/threonine kinase Akt mediates glucose-induced upregulation of collagen I in mesangial cells through transactivation of the EGF receptor (EGFR). In addition, in renal tubular cells, glucose-induced secretion of TGF-β requires phosphoinositide-3-OH kinase, suggesting a possible role for Akt in the modulation of TGF-β expression, but the mechanisms of Akt activation and its involvement in TGF-β regulation are unknown. Here, in primary mesangial cells, high glucose induced AktS473 phosphorylation, which correlates with its activation, in a protein kinase C β (PKC-β)-dependent manner. Glucose led to PKC-β1 membran..