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J. Biol. Chem., Vol. 276, Issue 19, 15913-15919, May 11, 2001
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From the Multiple intracellular signaling pathways have
been shown to regulate the hypertrophic growth of cardiac myocytes
including mitogen-activated protein kinase (MAPK) and
calcineurin-nuclear factor of activated T-cells. However, it is
uncertain if individual regulatory pathways operate in isolation or if
interconnectivity between unrelated pathways is required for the
orchestration of the entire hypertrophic response. To this end, we
investigated the interconnectivity between calcineurin-mediated cardiac
myocyte hypertrophy and p38 MAPK signaling in vitro and
in vivo. We show that calcineurin promotes down-regulation
of p38 MAPK activity and enhances expression of the dual specificity
phosphatase MAPK phosphatase-1 (MKP-1). Transgenic mice expressing
activated calcineurin in the heart were characterized by inactivation
of p38 and increased MKP-1 expression during early postnatal
development, before the onset of cardiac hypertrophy. In
vitro, cultured neonatal cardiomyocytes infected with a
calcineurin-expressing adenovirus and stimulated with phenylephrine
demonstrated reduced p38 phosphorylation and increased MKP-1 protein
levels. Activation of endogenous calcineurin with the calcium ionophore
A23187 decreased p38 phosphorylation and increased MKP-1 protein
levels. Inhibition of endogenous calcineurin with cyclosporin A
decreased MKP-1 protein levels and increased p38 activation in response
to agonist stimulation. To further investigate potential cross-talk
between calcineurin and p38 through alteration in MKP-1 expression, the
MKP-1 promoter was characterized and determined to be
calcineurin-responsive. These data suggest that calcineurin
enhances MKP-1 expression in cardiac myocytes, which is
associated with p38 inactivation.
Calcineurin Enhances MAPK Phosphatase-1 Expression and p38
MAPK Inactivation in Cardiac Myocytes*
,¶
Department of Pediatrics, University of
Cincinnati, Children's Hospital Medical Center, Cincinnati, Ohio
45229-3039 and the § Department of Immunology, The Scripps
Research Institute, La Jolla, California 92037
*
This work was supported by a National Institutes of
Health (NIH) grant, by the Pew charitable trust foundation (to
J. D. M., a Pew Scholar), and an NIH postdoctoral award (to
H. W. L).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.
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