[Role of Ca2+/calmodulin-dependent calcineurin signaling pathway in neuropeptide Y-induced cardiac hypertrophy in rats].
OBJECTIVE
To investigate the role of Ca(2+)/calmodulin-dependent calcineurin (CaN) signaling pathway in neuropeptide Y (NPY)-induced cardiomyocyte hypertrophy in rat.


METHODS
Cardiomyocytes 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.


RESULTS
Compared 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.


CONCLUSIONS
NPY can induce cardiomyocyte hypertrophy in rats, in which process Ca(2+)/calmodulin-dependent CaN signaling pathway plays an important role.
Li
Xiao-yun
XY
Department of Cardiology, Second Affiliated Hospital of Guangzhuo Medical College, Guangzhou 510260, China. yun530@sohu.com
Chen
Min-sheng
MS
Huang
Shao-hua
SH
Dong
Qin
Q
Li
Ying-hui
YH
Zhang
Shu
S
Liu
Zhen-xiu
ZX
D000818:Animals; D000831:Animals, Newborn; D019703:Calcineurin / Q000378:metabolism*; D002478:Cells, Cultured; D006984:Hypertrophy; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000473:pathology*; D009478:Neuropeptide Y / Q000494:pharmacology*; D016755:Proto-Oncogene Proteins c-jun / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D015398:Signal Transduction
D009478:Neuropeptide Y; D016755:Proto-Oncogene Proteins c-jun; D012333:RNA, Messenger; D019703:Calcineurin