TY - JOUR
T1 - The effects of the selective ROCK inhibitor, Y27632, on ET-1-induced hypertrophic response in neonatal rat cardiac myocytes - Possible involvement of Rho/ROCK pathway in cardiac muscle cell hypertrophy
AU - Kuwahara, Koichiro
AU - Saito, Yoshihiko
AU - Nakagawa, Osamu
AU - Kishimoto, Ichiro
AU - Harada, Masaki
AU - Ogawa, Emiko
AU - Miyamoto, Yoshihiro
AU - Hamanaka, Ichiro
AU - Kajiyama, Noboru
AU - Takahashi, Nobuki
AU - Izumi, Takehiko
AU - Kawakami, Rika
AU - Tamura, Naohisa
AU - Ogawa, Yoshihiro
AU - Nakao, Kazuwa
N1 - Funding Information:
We thank Ms. M. Okumura and Ms. M. Yamashita for their excellent secretarial work. We thank Dr. S. Narumiya for his kind gift of C3 and KD-IA, and Dr. D. G. Gardner for his pertinent advice on the transfection method. We also thank Dr. Sawada for his technical advice for the experiments using KD-IA. This work was supported in part by research grants from the Japanese Ministry of Education, Science and Culture; the Japanese Ministry of Health and Welfare; the Japanese Society for the Promotion of Science ‘Research for the Future’ program (JSPS-RFTF96I00204 and JSPS-RFTF98L00801); and the Smoking Research Foundation.
PY - 1999/6/11
Y1 - 1999/6/11
N2 - A small GTPase, Rho, participates in agonist-induced cytoskeletal organization and gene expression in many cell types including cardiac myocytes. However, little is known about the functions of Rho's downstream targets in cardiac myocytes. We examined the role of ROCK, a downstream target of Rho, in ET-1-induced hypertrophic response. Y27632, a selective ROCK inhibitor, inhibited ET-1-induced increases in natriuretic peptide production, cell size, protein synthesis, and myofibrillar organization. In addition, a dominant-negative mutant of p160ROCK suppressed ET-1-induced transcription of the BNP gene. These findings suggest that the Rho/ROCK pathway is an important component of ET-1-induced hypertrophic signals in cardiac myocytes. Copyright (C) 1999 Federation of European Biochemical Societies.
AB - A small GTPase, Rho, participates in agonist-induced cytoskeletal organization and gene expression in many cell types including cardiac myocytes. However, little is known about the functions of Rho's downstream targets in cardiac myocytes. We examined the role of ROCK, a downstream target of Rho, in ET-1-induced hypertrophic response. Y27632, a selective ROCK inhibitor, inhibited ET-1-induced increases in natriuretic peptide production, cell size, protein synthesis, and myofibrillar organization. In addition, a dominant-negative mutant of p160ROCK suppressed ET-1-induced transcription of the BNP gene. These findings suggest that the Rho/ROCK pathway is an important component of ET-1-induced hypertrophic signals in cardiac myocytes. Copyright (C) 1999 Federation of European Biochemical Societies.
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U2 - 10.1016/S0014-5793(99)00680-8
DO - 10.1016/S0014-5793(99)00680-8
M3 - Article
C2 - 10386613
AN - SCOPUS:0033005291
SN - 0014-5793
VL - 452
SP - 314
EP - 318
JO - FEBS Letters
JF - FEBS Letters
IS - 3
ER -