Function of protein kinase C (PKC) in the regulation of apoptosis related hyperglycemia in vascular smooth muscle cells.

糖尿病的共存加速了动脉粥样硬化的发生。高血糖是血管并发症发生的重要病因。(1)高糖对血管平滑肌细胞（VSMC）增殖和凋亡的影响。高糖显著促进VSMC细胞增殖，抑制凋亡诱导。(2) PKC同工酶过表达对VSMC细胞增殖和凋亡的影响。PKC-β 1过表达可刺激VSMC细胞增殖，抑制凋亡表达。相比之下，PKC-βII的过表达抑制了VSMC细胞的增殖并增加了细胞凋亡的诱导。(3)高糖对PKC同工酶和凋亡相关蛋白Bcl-xL和Bfl-1/A1表达的影响。与生理正常葡萄糖浓度处理的相同细胞相比，高葡萄糖处理导致CASMC细胞凋亡显著减少。与正常葡萄糖处理相比，高葡萄糖处理CASMC显著增加了bcl-xL和bfl-1/A1 mRNA的表达。高糖通过上调bcl-xL和bcl- 1/A1水平抑制细胞凋亡。高糖诱导的抗凋亡蛋白表达的增加可能在糖尿病患者动脉粥样硬化的发展中起重要作用。

Atherosclerosis is accelerated by the coexistence of diabetes mellitus. Hyperglycemia is an important etiologic factor in the development of vascular complications.(1) Effect of high glucose on cell proliferation and apoptosis in vascular smooth muscle cells (VSMC).High glucose stimulated cell proliferation and suppressed induction of apoptosis significantly in VSMC.(2) Effect of overexpression of PKC isozyme on cell proliferation and apoptosis in VSMC.Overexpression of PKC-βI stimulated cell proliferation and inhibited apoptosis expression in VSMC.In contrast, Overexpression of PKC-βII inhibited cell proliferation and increased induction of apoptosis in VSMC.(3) Effect of high glucose on the expression of PKC isozymes and apoptosis-related proteins, Bcl-xL and Bfl-1/A1.Treatment with a high glucose caused a significant decrease in apoptosis in CASMC compared with the same cells treated with a physiologically normal glucose concentration. Treatment of CASMC with high glucose concentration markedly increased mRNA expressions of bcl-xL and bfl-1/A1 compared with cells treated with normal glucose. High glucose suppressed apoptosis via upregulation of bcl-xL and bfl-1/A1 levels. High glucose-induced increase in the expression of antiapoptotic proteins may be important in the development of atherosclerosis in diabetic patients.