Ca~(2+)/calmodulin-dependent kinaseⅡare involved in tumor necrosis factor ?-induced cardiomyocyte hypertrophy in rats
- VernacularTitle:Ca~(2+)/CaMKⅡ信号通路在肿瘤坏死因子-?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-?;
calcium;
calmodulin-dependent kinase;
signal transduction;
KN93
- From:
Chinese Pharmacological Bulletin
1987;0(03):-
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate whether Ca2+/calmodulin-dependent kinase Ⅱ(CaMKⅡ)contribute to tumor necrosis factor ?(TNF-?)-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.[Ca2+]i transient was measured by Till image system by cell-loading Fura-2/AM.The expression of CaMKⅡ?B was determined by Western blot.Results ① TNF-? 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-? increased the amplitude of the spontaneous Ca2+ transients in cultured ventricular myocytes from the neonatal rat;CaMKⅡ inhibitor KN93 can suppress the elevation induced by TNF-?.③ TNF-? significantly increased the expression of CaMKⅡ?B.Concluslon CaMKⅡ signal pathway are involved in TNF-?-induced cardiomyocyte hypertrophy in rats.
