Publications by authors named "Daniel Ruggiero"
Advanced glycation end products (AGEs) are involved in the development of microvascular complications, including alterations of retinal pericyte and renal mesangial cell growth occurring during diabetic retinopathy and diabetic nephropathy, respectively. Because gangliosides are implicated in the regulation of cell proliferation, we hypothesized that AGEs could exert cellular effects in part by modulating ganglioside levels. Results of the present study indicate that AGEs caused an inhibition of both bovine retinal pericyte (BRP) and rat renal mesangial cell (RMC) proliferation, associated with an increase of a-series gangliosides consecutive to GM3 synthase activity increase and GD3 synthase activity inhibition.
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- Apoptosis, or programmed cell death, is likely the reason pericytes (a type of cell in the eye) are lost in diabetic retinopathy, a common eye problem for people with diabetes.
- In the study, scientists found that a substance called AGE-MGX causes pericytes to die by triggering certain biochemical changes in the cells.
- They discovered that caspases (special proteins that help the death process) play different roles, especially caspase-10, which could be a target for new treatments to help prevent eye damage in people with diabetes.
Endothelial damage is believed to play a key role in the development of both micro- and macrovascular disease in diabetes, and advanced glycation end products (AGEs) may contribute importantly to this. To determine whether glucose-derived AGEs can cause endothelial dysfunction, we examined the effects of albumin AGE-modified by glucose (AGE-Glu) both in vivo, after injection into rabbit femoral artery, and in vitro on rabbit aortic rings and cultured human umbilical vein endothelial cells (HUVEC). Exposure of blood vessels to AGE-Glu, in vivo and in vitro, inhibited endothelium-dependent vasorelaxation, whereas unmodified albumin did not.
View Article and Find Full Text PDFGlycation (nonenzymatic glycosylation of proteins) is known to be increased as a result of hyperglycaemia in diabetes. Moreover, cell glutathione concentration has been found to be lower in diabetics and such depletion may impair the cell defence against toxic radical species. Ribose being a potent reducing sugar expected to be increased in cells of diabetics where the pentose phosphate pathway is enhanced, its putative condensation with glutathione was investigated.
View Article and Find Full Text PDFArticle Synopsis
- Diabetic retinopathy starts with the loss of special cells in the eyes called pericytes, which protect tiny blood vessels.
- A study found that a substance called AGE can make these pericytes die by causing a cell process called apoptosis, and this is linked to increased levels of certain molecules called ceramide and diacylglycerol.
- Using antioxidants can stop this cell death, suggesting that it’s caused by stress in the cells, and researchers discovered new ways to target this problem for better treatments in diabetic retinopathy.