High glucose down-regulates the expression of miR-26b in H9C2 cardiomyocytes
10.16571/j.cnki.1008-8199.2019.02.007
- VernacularTitle: 高糖对H9C2心肌细胞miR⁃26b表达的影响
- Author:
Yu⁃sen ZHOU
1
;
Ya⁃ping ZHAO
2
;
Chao ZHAO
2
;
Guang⁃feng XU
2
;
Nai⁃jian ZHANG
2
;
Chun⁃hui WANG
3
Author Information
1. Department of Postgraduate Students, Bengbu Medical College, Bengbu 233000, Anhui, China
2. Department of Clinical Laboratory, The 82nd Hospital of General Hospital of Eastern Theater Command, PLA, Huai′an 223001, Jiangsu, China
3. Department of Cardiology, The 82nd Hospital of General Hospital of Eastern Theater Command, PLA, Huai′an 223001, Jiangsu, China
- Publication Type:Journal Article
- Keywords:
glucose;
miR⁃26b;
cardiomyocytes;
diabetic cardiomyopathy
- From:
Journal of Medical Postgraduates
2019;32(2):148-152
- CountryChina
- Language:Chinese
-
Abstract:
Objective Diabetic cardiomyopathy (DCM) is one of the complications of diabetes, which is closely related to the change of miRNA. In this study, we observed the characteristic expression of miR-26b in the tissues of the C57BL/6J mouse and in the heart, adipose tissue and liver of the ob/ob mouse, and investigated the effect of high glucose (Glu) on the expression of miR-26b in H9C2 cardiomyocytes. Methods Using RT-PCR, we measured the levels of miR-26b in the heart, adipose tissue, liver and other tissues of C57BL/6J and ob/ob mice. H9C2 cardiomyocytes were treated with Glu at 5.5, 15, 25 and 35 mmol/L for 0, 24, 48, 72, 96 and 120 hours, followed by detection of the proliferation of cardiomyocytes by CCK-8 and determination of thelevels miR-26b. Results The expression of miR-26b was the highest in the heart of the C57BL/6J mice, significantly higher than in the cardiac and white adipose tissues of the ob/ob mice (P < 0.05). The proliferation of cardiomyocytes was markedly increased in the 15, 25 and 35 mmol/L Glu groups at 24, 48, 72, 96 and 120 hours as compared with that in the 5.5 mmol/L Glu group (P < 0.05), higher in the 25 than in the 15 mmol/L Glu group at 24 hours (0.74±0.02 vs 0.72±0.01, P<0.05), but lower in the 35 than in the 15 mmol/L Glu group at 48 hours (0.92±0.01 vs 0.94±0.01, P<0.05), in the 25 and 35 mmol/L Glu groups at 96 hours (P < 0.05), in the 35 mmol/L Glu group at 120 hours (1.12±0.02 vs 1.19±0.05, P<0.05), in the 35 than in the 25 mmol/L Glu group at 24 and 48 hours (P<0.05). The expression of miR-26b in the H9C2 cardiomyocytes was significantly down-regulated in the 25 and 35 mmol/L Glu groups in comparison with that in the 5.5 mmol/L Glu group (P<0.05), remarkably lower in the 25 mmol/L Glu group at 96 and 120 hours than at 0 hour (P<0.05). Conclusion High glucose can down-regulate the expression of miR-26b in H9C2 cardiomyocytes, which suggests that miR-26b may participate in the pathogenesis of DCM.
