Calcineurin contributed to tumor necrosis factor alpha-induced cardiomyocyte hypertrophy in rats.
- Author:
Gui-Jun WANG
1
;
Yu-Sheng YAO
;
Hong-Xin WANG
;
Lian-Yi GUO
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Calcineurin; metabolism; Calcium Signaling; Cardiomyopathy, Dilated; metabolism; pathology; Cells, Cultured; Female; Male; Myocytes, Cardiac; drug effects; metabolism; pathology; Rats; Rats, Sprague-Dawley; Tumor Necrosis Factor-alpha; pharmacology
- From: Chinese Journal of Applied Physiology 2012;28(2):184-188
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate whether calcineurin (CaN) contribute to tumor necrosis factor alpha (TNF-alpha)-induced cardiomyocyte hypertrophy.
METHODSThe 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]-leucine incorporation method. [Ca2+]i transient was measured by Till image system by cell-loading Fura-2/AM. The expression of CaN was determined by Western blot.
RESULTS(1) (CsA (0.2 micromol/L), a selective CaN inhibitor, significantly suppressed the increase of protein content, [3H]-leucine incorporation and cell size induced by TNF-alpha. (2) CsA (0.2 micromol/L) significantly suppressed the elevation of the amplitude of the spontaneous Ca2+ transients induced by TNF-alpha in cultured ventricular myocytes from the neonatal rat. (3) TNF-alpha significantly increased the expression of CaN.
CONCLUSIONCa(2+) -CaN signaling pathway are involved in cardiomyocyte hypertrophy induced by TNF-alpha in rats.
