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Originally published In Press as doi:10.1074/jbc.M100699200 on May 29, 2001

J. Biol. Chem., Vol. 276, Issue 31, 29490-29498, August 3, 2001
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A Role for the Extracellular Signal-regulated Kinase and p38 Mitogen-activated Protein Kinases in Interleukin-1beta -stimulated Delayed Signal Tranducer and Activator of Transcription 3 Activation, Atrial Natriuretic Factor Expression, and Cardiac Myocyte Morphology*

Dominic C. H. NgDagger , Carlin S. Long§, and Marie A. BogoyevitchDagger ||

From the Dagger  Department of Biochemistry, University of Western Australia, Crawley 6009, Australia, the § Cardiology Section, Denver Health Medical Center and the University of Colorado, Denver, Colorado 80204, and the  Western Australian Institute for Medical Research, Perth, Western Australia 6000, Australia

We have demonstrated that two hypertrophic agents, interleukin-1beta (IL-1beta ) and leukemic inhibitory factor (LIF), altered cardiac myocyte morphology with striking similarity and prompted us to investigate the common actions of these cytokines. We compared the phosphorylation/activation of signal tranducer and activator of transcription 3 (STAT3), extracellular signal-regulated kinase (ERK), p38MAPK, and c-Jun N-terminal kinase mitogen-activated protein kinases (MAPKs). The phosphorylation of STAT3 by IL-1beta was delayed (>60 min), whereas the response to LIF was rapid (<10 min) and transient. We confirmed that IL-1beta potently stimulated all three MAPK subfamilies. In contrast, LIF promoted strong activation of ERKs, marginal activation of p38MAPK, and no c-Jun N-terminal kinase activation. To test the roles of ERKs and p38MAPK, myocytes were pretreated with PD98059 and SB203580. Either inhibitor alone prevented STAT3 phosphorylation, implicating ERKs and p38MAPK in the delayed STAT3 response to IL-1beta . The interplay of MAPKs and STAT3 phosphorylation in regulating IL-1beta -stimulated hypertrophy was investigated by evaluating the effect of MAPK inhibitors on atrial natriuretic factor (ANF) expression and myocyte morphology. The specific inhibition of either ERK or p38MAPK attenuated the IL-1beta - or LIF-stimulated ANF expression by up to 70%. Inhibition was not further increased in the presence of both inhibitors. Furthermore, although individual inhibition of ERK or p38MAPK did not affect morphology, co-treatment with both inhibitors abrogated the hypertrophic morphology stimulated by IL-1beta but not by LIF. Taken together, our data indicate that the activation of ERK and p38MAPK is essential in regulating a delayed STAT3 phosphorylation as well as changes in ANF expression and morphology that follow IL-1beta treatment. Thus, the role of MAPKs in the hypertrophic response can be dictated at least partly by the nature of the hypertrophic agent employed.

* This work was supported by the Australian National Heart Foundation and the Department of Industry, Science, and Technology Bilateral Collaboration Scheme. The Confocal Laser Scanning Microscopy Facility at the University of Western Australia is supported by the Lotteries Commission of Western Australia.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

|| To whom correspondence should be addressed: Cell Signaling Laboratory, Dept. of Biochemistry, University of Western Australia, 35 Stirling Hwy., Crawley, Western Australia 6009, Australia. Tel.: 61-8-9380-1348; Fax: 61-8-9380-1148; E-mail: marieb@cyllene.uwa.edu.au.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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