A study on mechanisms of CaMKII mediated 20-HETE-induced apoptosis in neonatal rat cardiomyocytes
10.3969/j.issn.1006-5725.2018.04.002
- VernacularTitle:CaMKII介导20-HETE诱导的乳鼠心肌细胞凋亡作用机制研究
- Author:
Yan HE
1
;
Chanyi JIA
;
Chuyi HAN
;
Hongbao HOU
;
Yuanshou CHEN
;
Yong HAN
Author Information
1. 遵义医学院生理教研室 贵州遵义563000
- Keywords:
20-HETE;
CaMKII;
apoptosis;
calcium overload
- From:
The Journal of Practical Medicine
2018;34(4):521-526
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the effect of 20-HETE on apoptosis in cultured neonatal rat cardiomyo-cytes and investigate its mechanism. Methods Neonatal rat cardiomyocytes were cultured in vitro.CCK-8 method was used to detect the cell activity and TUNEL assay was performed to analyze the cell apoptosis. Flou-3/AM la-belled assay was applied to measure the concentration of intracellular calcium([Ca2+]i). Western blot was per-formed to measure the expressions of RyR2,SERCA2a,CaMKII and phospho-CaMKII. Results Treatment with 20-HETE reduced the activity of cardiomyocytes and induced cell apoptosis obviously,while KN-93,an inhibitor of CaMKII,blocked the effects of 20-HETE. Treatment with 20-HETE significantly increased cardiomyocytes [Ca2+]i,up-regulated the expression of RyR2,and down-regulated the expression of SERCA2a,which could be blocked by KN-93. 20-HETE also increased the expressions of CaMKII and phospho-CaMKII in cardiomyocytes, indicating 20-HETE played a role in activating the CaMKII signaling pathway. Conclusions 20-HETE leads to altered functions of cardiac sarcoplasmic reticulum calcium-transport protein RyR2 and SERCA2a via activating the CaMKII signaling pathway,which causes calcium overload and induces apoptosis in neonatal rat cardiomyocytes.
