Circulation. 2002;105:509-515
doi: 10.1161/hc0402.102863
doi: 10.1161/hc0402.102863
(Circulation. 2002;105:509.)
© 2002 American Heart Association, Inc.
Basic Science Reports |
Involvement of Nuclear Factor-
B and Apoptosis Signal-Regulating Kinase 1 in G-Protein–Coupled Receptor Agonist–Induced Cardiomyocyte Hypertrophy
From the Department of Pathophysiology (S.H., K.N., T. Morita, M.T.), Department of Internal Medicine and Therapeutics (K.O., Y.H., H.N., O.Y., T. Mano, M.H.), and Department of Medical Information Science (Y.M.), Osaka University Graduate School of Medicine, Osaka, and Department of Biochemistry and Molecular Pathophysiology (H.U.), University of Occupational and Environmental Health, School of Medicine, Kitakyushu, Japan.
Correspondence to Kinya Otsu, Department of Pathophysiology, Box H2, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan. E-mail kotsu{at}medone.med.osaka-u.ac.jp
Background— Recently, reactive oxygen species (ROS) have emerged as important molecules in cardiac hypertrophy. However, the ROS-dependent signal transduction mechanism remains to be elucidated. In this study, we examined the role of an ROS-sensitive transcriptional factor, NF-
B, and a mitogen-activated protein kinase kinase kinase, apoptosis signal-regulating kinase 1 (ASK1), in G-protein–coupled receptor (GPCR) agonist (angiotensin II, endothelin-1, phenylephrine)-induced cardiac hypertrophy in isolated rat neonatal cardiomyocytes.
Methods and Results— Using an ROS-sensitive fluorescent dye, we observed an increase in fluorescence signal on addition of the GPCR agonists. The GPCR agonists induced NF-B activation. Antioxidants such as N-acetyl cysteine, N-mercaptopropionyl glycine, and vitamin E attenuated the NF-B activation. Infection of cardiomyocytes with an adenovirus expressing a degradation-resistant mutant of IB
led to suppression of the hypertrophic responses. The GPCR agonists rapidly and transiently activated ASK1 in a dose-dependent manner. Infection of an adenovirus expressing a dominant-negative ASK1 attenuated the GPCR agonist–induced NF-B activation and cardiac hypertrophy. Overexpression of a constitutively active mutant of ASK1 led to NF-B activation and cardiac hypertrophy. Activated ASK1-induced hypertrophy was abolished by inhibition of NF-B activation.
Conclusions— These data indicate that GPCR agonist–induced cardiac hypertrophy is mediated through NF-B activation via the generation of ROS. ASK1 is involved in GPCR agonist–induced NF-B activation and resulting hypertrophy.
Key Words: hypertrophy • myocytes • signal transduction • free radicals
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