Ca~(2+)/calmodulin-dependent kinaseⅡare involved in tumor necrosis factor α-induced cardiomyocyte hypertrophy in rats
- VernacularTitle:Ca~(2+)/CaMKⅡ信号通路在肿瘤坏死因子-α诱导心肌肥大中的作用
- Author:
Guijun WANG
;
Yusheng YAO
;
Hongxin WANG
- Publication Type:Journal Article
- Keywords:
cardiomyocyte hypertrophy;
tumor necrosis factor-α;
calcium;
calmodulin-dependent kinase;
signal transduction;
KN93
- From:
Chinese Pharmacological Bulletin
2010;26(3):387-391
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate whether Ca~(2+)/calmodulin-dependent kinase Ⅱ(CaMKⅡ)contribute to tumor necrosis factor α(TNF-α)-induced cardiomyocyte hypertrophy.Methods The protein content was assayed with Lowry's method.The cardiomyocytes volumes were measured by computer photograph analysis system.The protein synthesis was assayed with[~3H]-lencine incorporation method.[Ca~(2+)]_i transient was measured by Till image system by cell-loading Fura-2/AM.The expression of CaMKⅡδ_B was determined by Western blot.Results ① TNF-α significantly induced the increase of protein content, [~3H]-leucine incorporation and cell size;These responses were significantly suppressed by KN93, a selective CaMKⅡ inhibitor.② TNF-α increased the amplitude of the spontaneous Ca~(2+) transients in cultured ventricular myocytes from the neonatal rat;CaMKⅡ inhibitor KN93 can suppress the elevation induced by TNF-α.③ TNF-α significantly increased the expression of CaMKⅡδ_B.Concluslon CaMKⅡ signal pathway are involved in TNF-α-induced cardiomyocyte hypertrophy in rats.
