Activation of calcium-sensing receptors is associated with apoptosis in cardiomyocytes under simulated ischemia/reperfusion.
- Author:
Ling YAN
1
;
Tie-Bing ZHU
;
Ting-Ting SUN
;
Shi-Yang PAN
;
Lain-Sheng WANG
;
Zheng-Xian TAO
;
Zhi-Jian YANG
;
Ke-Jiang CAO
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; physiology; Caspase 3; metabolism; Cells, Cultured; Myocardial Reperfusion Injury; metabolism; pathology; Myocytes, Cardiac; metabolism; pathology; Proto-Oncogene Proteins c-bcl-2; metabolism; Rats; Receptors, Calcium-Sensing; metabolism; Signal Transduction
- From: Journal of Zhejiang University. Medical sciences 2011;40(2):207-212
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo examine the association of activation of calcium-sensing receptors (CaSR) with apoptosis in cardiomyocytes under simulated ischemia/reperfusion.
METHODSVentricular cardiomyocytes of neonatal rats were incubated in ischemia-mimetic solution for 2 h, then re-incubated in normal culture medium for 24 h to establish a model of simulated ischemia/reperfusion (I/R). Cell apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL assay). The expression of CaSR mRNA was detected by reverse transcriptase polymerase chain reaction (RT-PCR). The expression of Caspase -3 and Bcl-2 was detected by Western blotting.
RESULTThe simulated I/R enhanced the expression of CaSR and cardiomyocyte apoptosis. GdCl(3), a specific activator of CaSR, further increased the expression of CaSR and cardiomyocyte apoptosis, along with upregulation of Caspase-3 and downregulation of Bcl-2.
CONCLUSIONCaSR is associated with I/R injury and apoptosis in neonatal rat ventricular cardiomyocytes via suppressing Bcl-2 and promoting Caspase -3 expression.
