From the Department of Medicine III, Osaka University Medical School,
Japan.
Correspondence to Keiko Yamauchi-Takihara, MD, PhD, Department of Medicine III, Osaka University Medical School, 2-2 Yamadaoka, Suita, Osaka 565, Japan. E-mail takihara{at}imed3.med.osaka-u.ac.jp
Background—gp130, a signal
transducer of the IL-6–related cytokines, is expressed
ubiquitously, including in the heart. The activation of gp130 in
cardiac myocytes was reported to induce myocardial
hypertrophy. The downstream side of gp130 consists of two
distinct pathways in cardiac myocytes, one a Janus kinase/signal
transducer and activator of transcription (JAK/STAT)
pathway, the other a mitogen-activated protein kinase (MAPK)
pathway. In the present study, we examined whether the JAK/STAT
pathway, especially the STAT3-mediated pathway, plays a critical role
in gp130-dependent myocardial hypertrophy by transfecting
wild-type and mutated-type STAT3 cDNA to cardiac myocytes.
Methods and Results—We constructed three kinds of
replication-defective adenovirus vectors carrying wild-type (AD/WT) or
mutated-type (AD/DN) STAT3 cDNA or adenovirus vector itself (AD).
Cultured murine cardiac myocytes infected with adenovirus were
stimulated with leukemia inhibitory factor (LIF), and the
expression of c-fos and atrial natriuretic
factor (ANF) mRNAs and [3H]leucine
incorporation were examined. There were no significant differences in
MAPK activity among the three groups. Compared with AD-transfected
cardiac myocytes, induction of c-fos and ANF
mRNAs and protein synthesis after LIF stimulation were significantly
augmented in AD/WT-transfected cells. In contrast, induction of
c-fos and ANF mRNA expression and protein
synthesis were attenuated after LIF stimulation in cardiac myocytes
transfected with AD/DN.
Conclusions—These results suggest that the STAT3-dependent
signaling pathway downstream of gp130 promotes cardiac myocyte
hypertrophy under stimulation with LIF.
© 1998 American Heart Association, Inc.
Basic Science Reports
Activation of gp130 Transduces Hypertrophic Signals via STAT3 in Cardiac Myocytes
Key Words: interleukins • hypertrophy • signal transduction • STAT3 • myocytes
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