Ca2+ is involved in tumor necrosis factor-alpha induced cardiomyocyte hypertrophy through PI3-kinase pathway in rats.
- Author:
Gui-Jun WANG
1
;
Yu-Sheng YAO
;
Zhuang-Peng LI
;
Hong-Xin WANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Calcium; metabolism; Calcium Channels, L-Type; metabolism; Chromones; pharmacology; Female; Hypertrophy; Male; Morpholines; pharmacology; Myocytes, Cardiac; drug effects; metabolism; pathology; Phosphatidylinositol 3-Kinases; metabolism; Rats; Rats, Sprague-Dawley; Signal Transduction; Tumor Necrosis Factor-alpha; pharmacology
- From: Chinese Journal of Applied Physiology 2010;26(3):284-288
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate whether Ca2+ contribute to cardiomyocyte hypertrophy induced by tumor necrosis factor-alpha (TNF-alpha) through PI3-kinase pathway.
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.
RESULTS(1) TNF-alpha significantly induced the increase of protein content, [3H]-leucine incorporation and cell size. These responses were significantly suppressed by LY294002, a selective PI3-kinase inhibitor. Verapamil, L-type calcium channels antagonist, slightly attenuated TNF-alpha-induced these responses. (2) TNF-alpha increased the amplitude of the spontaneous Ca2+ transients in cultured ventricular myocytes from the neonatal rat; PI3-kinase inhibitor LY294002 could suppress the elevation induced by TNF-alpha, but calcium antagonist verapamil took the minor effects of TNF-alpha on [Ca2+]i metabolism.
CONCLUSIONIncreasing the intercellular free Ca2+ level may play an essential role in TNF-alpha-induced cardiomyocyte hypertrophy through PI3-kinase pathway in rats, while L-type calcium channel takes the minor effects on it.
