[Involvement of calcineurin-dependent signal pathway in the angiotensin II-induced cardiac myocyte hypertrophy].
The present study was undertaken to observe the role of calcineurin (CaN)-dependent signaling pathway in the angiotensin II (Ang II)-induced cardiac myocyte hypertrophy. In cultured myocardial cells of neonatal rats, Ang II was used to stimulate hypertrophy and CaN-pathway blocked by CsA(an inhibitor of CaN). 3H-leucine incorporation, and activities of CaN, mitogen-activated protein kinase (MAPK) and protein kinase C (PKC) were investigated. The results showed that 3H-leucine incorporation of Ang II-stimulated myocardial cells was 46% higher than control (P < 0.01), which could be inhibited by CsA (0.5-5 micrograms/ml) and PD098059(an inhibitor of MAPK). CaN and PKC activities of Ang II-stimulated myocardial cells were 39% and 280% higher than control (P < 0.001) respectively, while no significant increase in MAPK activities was observed. CsA could reverse the increase of CaN activity, but had no effect on PKC. It is concluded that the CaN-dependent signaling pathway may play an important role in the development of the Ang II-induced cardiac myocyte hypertrophy.
Fu
M G
MG
Institute of Cardiovascular Research, First Hospital, Beijing Medical University, Beijing 100034.
Wang
X H
XH
Jiang
Z S
ZS
Pang
Y Z
YZ
Liu
N K
NK
Tang
C S
CS
D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D019703:Calcineurin / Q000502:physiology*; D006332:Cardiomegaly / Q000139:chemically induced / Q000503:physiopathology*; D002478:Cells, Cultured; D016572:Cyclosporine / Q000494:pharmacology; D009206:Myocardium / Q000166:cytology*; D051381:Rats; D015398:Signal Transduction
D000804:Angiotensin II; D016572:Cyclosporine; D019703:Calcineurin