MicroRNA-34a Regulates High Glucose-induced Apoptosis in H9c2 Cardiomyocytes

• Published in: Journal of Huazhong University of Science and Technology. Medical sciences Vol. 33; no. 6; pp. 834 - 839
• Main Author: 赵芳 李波 卫银芝 周斌 汪瀚 陈明 干学东 汪朝晖 熊世熙
• Format: Journal Article
• Language: English
• Published: Heidelberg Huazhong University of Science and Technology 01.12.2013; Department of Cardiovascular Diseases, Zhongnan Hospital of Wuhan University, Wuhan 430071, China%Department of Oral Radiology, School and Hospital of Stomatology, Wuhan University, Wuhan 430079, China
• Subjects: Animals; Apoptosis; Bcl-2基因; Bcl-2蛋白; Cell Line; Glucose - metabolism; Medicine; Medicine & Public Health; MicroRNAs - genetics; MicroRNAs - metabolism; Myocytes, Cardiac - metabolism; Rats; Western印迹法; 心肌细胞凋亡; 糖尿病并发症; 诱导凋亡; 调控; 高糖; Bcl-2; apoptosis; high glucose; miR-34a
• ISSN: 1672-0733; 1993-1352
• DOI: 10.1007/s11596-013-1207-7

Hyperglycemia is an important initiator of cardiovascular disease, contributing to the de- velopment of cardiomyocyte death and diabetic complications. The purpose of the present study was to investigate whether high glucose state could induce apoptosis of rat cardiomyocyte cell line H9c2 through microRNA-mediated Bcl-2 signaling pathway. The expression of miR-34a and Bcl-2 mRNA was detected by using real-time PCR. Western blotting was used to examine the changes in apop- tosis-associated protein Bcl-2. Apoptosis of H9c2 cells was tested by using flow cytometry. The results showed that the expression of miR-34a was significantly elevated and that of Bcl-2 was strongly re- duced, and apoptosis of cardiomyocytes was apparently increased in the high-glucose-treated H9c2 cells as compared with normal-glucose-treated controls. In addition, we identified Bcl-2 gene was the target of miR-34a, miR-34a mimics reduced the expression of Bcl-2 and increased glucose-induced apoptosis, but miR-34a inhibitor acted as the opposite mediator. Our data demonstrate that miR-34a contributes to high glucose-induced decreases in Bcl-2 expression and subsequent cardiomyocyte apoptosis.