[The biochemical mechanism in vitro of pericyte drop-out in diabetic retinopathy].
An experimental pathologic model of pericyte drop-out was established with capillary pericytes in culture medium of high glucose concentration. The high glucose activated the sorbitol pathway, reduced the intracellular myo-inositol content and disturbed the inositol phospholipid metabolism which resulted in a decrease in the inositol trisphosphate (IP3) level. The correlation of suppressed IP3 level with reduced DNA synthesis was evident, suggesting the mechanism that retinal pericytes degenerated in high glucose concentration. In vitro test of adding myo-inositol and/or aldose reductase inhibitor to the high-glucose medium reversed the inositol phospholipid metabolism and the decreased DNA synthesis, which could hold promise for the clinical prevention and treatment of early diabetic retinopathy.
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D000818:Animals; D002417:Cattle; D002470:Cell Survival; D002478:Cells, Cultured; D004247:DNA / Q000096:biosynthesis; D003930:Diabetic Retinopathy / Q000378:metabolism / Q000473:pathology*; D015544:Inositol 1,4,5-Trisphosphate / Q000378:metabolism
D015544:Inositol 1,4,5-Trisphosphate; D004247:DNA