Abstract

It has been suggested that decrease in the number of glomerular cells, including mesangial cells, occurs in the process of developing diabetic glomerulosclerosis. On the other hand, formation of methylglyoxal (MG), a highly reactive dicarbonyl compound, is accelerated through several pathways including the glycation reaction under diabetic conditions, presumably contributing to tissue injury in diabetes. We therefore examined if MG was capable of inducing cell death by apoptosis using cultured rat mesangial cells (RMC). Incubation of RMC with MG resulted in the dose-dependent induction of apoptosis, which was evaluated by both TUNEL analysis and detection of DNA laddering. These findings suggest that MG may play a potential role in the development of diabetic glomerulosclerosis through apoptosis of glomerular mesangial cells.

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