Ca~(2+)/calmodulin-dependent kinaseⅡare involved in tumor necrosis factor α-induced cardiomyocyte hypertrophy in rats / 中国药理学通报
Chinese Pharmacological Bulletin
; (12): 387-391, 2010.
Artigo
em Chinês
| WPRIM (Pacífico Ocidental)
| ID: wpr-403234
Biblioteca responsável:
WPRO
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.
Texto completo:
Disponível
Base de dados:
WPRIM (Pacífico Ocidental)
Idioma:
Chinês
Revista:
Chinese Pharmacological Bulletin
Ano de publicação:
2010
Tipo de documento:
Artigo