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Articles in PresS, published online ahead of print April 18, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00577.2001
Submitted on December 2, 2001
Accepted on March 28, 2002
1 Third Department of Internal Medicine, Gifu University, School of Medicine, Gifu, Gifu, Japan
* To whom correspondence should be addressed. E-mail: myamamot{at}cc.gifu-u.ac.jp.
Cardiovascular disease is a serious complication in diabetic patients. To elucidate the precise mechanisms of atherosclerosis in diabetic patients, the effects of a high glucose (25 mmol/L) on apoptosis regulation and bcl-2 family protein expression in human coronary artery smooth muscle cells (CASMC) were examined. Treatment with high level of glucose (25 mM) caused a significant decrease in apoptosis in CASMC as compared with the same cells treated with physiologically normal glucose concentration (5.5 mmol/L) (23.9±2.4 vs. 16.5±1.8%, p<0.01). With respect to apoptosis regulation, treatment of CASMC with high glucose markedly increased mRNA expressions of bcl-xL and bfl-1/A1 compared to cells treated with normal glucose. High glucose induced phosphorylation of phosphatidylinositol 3-kinase (PI 3-K) and extracellular-response kinase (ERK1/2) along with bcl-xL and bfl-1/A1 up regulation. These results suggest that high glucose suppresses apoptosis via up-regulation of bcl-xL and bfl-1/A1 levels through PI 3-K and ERK1/2 pathways in CASMC. High glucose induced increase in the expression of anti-apoptotic proteins may be important in the development of atherosclerosis in diabetic patients.
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