Effect of calcineurin Aalpha gene overexpression on the myocardium apoptosis induced by hypoxia-reoxygenation and adrenergic receptors.
- Author:
Xiao-mei SHEN
1
;
Ju-yan ZHANG
;
Bei CHENG
Author Information
- Publication Type:Journal Article
- MeSH: Adenoviridae; genetics; Adrenergic beta-Agonists; pharmacology; Animals; Animals, Newborn; Apoptosis; drug effects; genetics; physiology; Blotting, Western; Calcineurin; genetics; metabolism; Cell Hypoxia; Cells, Cultured; Female; Flow Cytometry; Genetic Vectors; genetics; Isoproterenol; pharmacology; Male; Myocytes, Cardiac; cytology; drug effects; metabolism; Oxygen; pharmacology; Phosphorylation; drug effects; RNA, Messenger; genetics; metabolism; Rats; Rats, Wistar; Receptors, Adrenergic; physiology; Reverse Transcriptase Polymerase Chain Reaction; Transfection; p38 Mitogen-Activated Protein Kinases; metabolism
- From: Journal of Southern Medical University 2006;26(11):1633-1636
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of calcineurin AalphacDNA (AdCnAalpha) overexpression as a result of adenovirally mediated gene transfer on neonatal rat cardiac myocyte apoptosis induced by hypoxia-reoxygenation (H/R) and adrenergic receptors.
METHODSNeonatal rat cardiac myocytes were cultured for 20 h after AdCnAalpha transfection, and treated with isoproterenol (10 micromol/L) and 24 h of hypoxia followed by 4 h of reoxygenation (24H/4R). The cardiac myocyte apoptosis induced by the treatments was assessed by flow cytometry and DNA laddering, and the levels of calcineurin, p38 and phosphorylation p38 (p-p38) were determined by Western blotting and (or) RT-PCR.
RESULTSAdCnAalpha transfection promoted cultured neonatal rat cardiac myocyte apoptosis induced by isoproterenol+24H/4R as compared with the treated cells without transfection (14.247-/+0.525 vs 10.763-/+1.554, P<0.01), along with greater phosphorylation p38 protein expression (1.60-/+0.22 vs 2.42-/+0.19, P<0.01). The levels of p38 underwent no obvious change after AdCnAalpha transfection (P<0.05).
CONCLUSIONSAdCnAalpha transfection can promote cardiac myocyte apoptosis induced by H/R and adrenergic receptors, the mechanism of which might be associated with p38 mitongen-activated protein kinase (p38MAPK) activation.
