PKC signaling and consequent TGF-beta 1 activation participate in the glycated albumin-induced stimulation of basement membrane collagen production by GEnC. By reducing the proliferative capacity, which is likely mediated by PKC and partly by TGF-beta, glycated albumin impedes the ability of the glomerular capillary endothelium to act as a first line of defense against deleterious circulating factors in the diabetic state.
The findings causally implicate the increased glycated albumin associated with the diabetic state in the abnormal renal nephrin and VEGF expression found in diabetes, thereby promoting proteinuria and glomerulosclerosis.
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