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Cyclin D2 is involved in the pathology of vascular complications of type 2 diabetes mellitus (T2DM).This study investigated the role of cyclin-D2-regulated miRNAs in endothelial cell proliferation of T2DM.Results showed that high glucose concentration (4.5 g/L) significantly promoted the proliferation of rat aortic endothelial cells (RAOECs) and significantly increased the expression of cyclin D2 and phosphorylation of RB1 (p-RB1) in RAOECs compared with those under low glucose concentration.Similarly, cyclin D2 and p-RB 1 levels remarkably increased in endothelial cells of established streptozotocin-induced diabetic rat model aortas compared with those in healthy control rats.The cyclin D2-3 untranslated region is targeted by miR-98, as evidenced by miRNA analysis software.Western blot also confirmed that cyclin D2 expression decreased in miR-98-treated RAOECs compared with that in control oligo treatment.The expression levels of miR-98 decreased in 4.5 g/L glucose-treated cells compared with those treated by low glucose concentration, as supported by real-time quantitative PCR data.The expression of miR-98 also significantly decreased in endothelial cells of diabetic aortas compared with that in healthy control rats.Furthermore, the results indicated that miR-98 can induce RAOEC apoptosis.The suppression of RAOEC growth by miR-98 might be related to the regulation of Bcl-2, Bax, and caspase-9 expression.In conclusion, this study demonstrated that high glucose concentration induces cyclin D2 overexpression and miR-98 downregulation in RAOECs.By regulating cyclin D2, miR-98 can inhibit human endothelial cell growth, thereby providing novel therapeutic targets for vascular complications of T2DM.