Role of Ca2+/calmodulin-dependent calcineurin signaling pathway in neuropeptide Y-induced cardiac hypertrophy in rats.
- Author:
Xiao-yun LI
1
;
Min-sheng CHEN
;
Shao-hua HUANG
;
Qin DONG
;
Ying-hui LI
;
Shu ZHANG
;
Zhen-xiu LIU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Animals, Newborn; Calcineurin; metabolism; Cells, Cultured; Hypertrophy; Myocytes, Cardiac; metabolism; pathology; Neuropeptide Y; pharmacology; Proto-Oncogene Proteins c-jun; genetics; metabolism; RNA, Messenger; genetics; metabolism; Rats; Rats, Wistar; Signal Transduction
- From: Journal of Southern Medical University 2008;28(12):2139-2141
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the role of Ca(2+)/calmodulin-dependent calcineurin (CaN) signaling pathway in neuropeptide Y (NPY)-induced cardiomyocyte hypertrophy in rat.
METHODSCardiomyocytes of neonatal Wistar rats were cultured in the presence of 10 and 100 nmol/L NPY, and cyclosporine A (CsA) was applied to inhibit the activity of CaN. The protein synthesis rate, c-jun mRNA expression, CaN protein expression, CaN activity and intracellular Ca(2+) concentration in the cardiomyocytes were assessed.
RESULTSCompared with the control group, (3)H-Leu incorporation and expression of c-jun mRNA in the cardiomyocytes treated with 100 nmol/L NPY increased significantly (P<0.05, P<0.001), and the effect of NPY was blocked by CsA. The activity of CaN (P<0.05), CaN expression (P<0.05), and Ca(2+) concentration in the cytoplasm (P<0.001) and nuclei (P<0.001) of the cells with 100 nmol/L NPY treatment also significantly increased compared with those in the control cells.
CONCLUSIONNPY can induce cardiomyocyte hypertrophy in rats, in which process Ca(2+)/calmodulin-dependent CaN signaling pathway plays an important role.
