Apoptosis and proliferation in diabetic eyes

Abstract

AbstractPurpose Diabetic retinopathy (DR) is the most common cause of visual loss in the working population and the incidence of diabetes is increasing. In addition, 80% of diabetic patients will show some form of retinopathy after 15 years, even with good glycaemic control. The mechanism of diabetic retinopathy is still not fully understood although hyperglycaemia is the main determinant. Diabetes appears to have contradictory effects on vasculature, causing reduced angiogenesis or increased angiogenesis at different vascular sites.Methods The effect of high glucose (HG) on in vitro proliferation, apoptosis and angiogenesis of retinal endothelial cells was investigated using relevant assays. Real time PCR was used to quantify signalling responses to high glucose through gene expression of key signalling molecules such as HIF and expression of VEGF.Results HG conditions reduced the proliferation of retinal endothelial cells but no increase in apoptosis was detected, and increased VEGF prevented this response. Gene expression of HIF was increased with HG and that of VEGF decreased dependent on glucose concentration and exposure time.Conclusion Contrary to other research in this area we found that apoptosis may not play the major role in the early phase of DR, and that reduced endothelial cell proliferation precedes apoptosis. Angiogenic signalling induced by hyperglycaemia is complex and requires further elucidation. Commercial interest