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J. Biol. Chem., Vol. 277, Issue 32, 28942-28947, August 9, 2002
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From the Department of Pediatrics, Divisions of
In myocytes, calcium plays an important role in
intracellular signaling and contraction. However, the ability of
calcium to modulate the differentiation of striated muscle cells is
poorly understood. To examine this issue we studied C2C12 cells, which is a myoblast cell line that differentiates in vitro.
First, we observed that the L-type calcium channel blockers nifedipine
and verapamil effectively inhibited electrically induced calcium
transients. Next, C2C12 cells were exposed to these agents during
conditions that induce myocyte differentiation. In the presence of
nifedipine and verapamil, myoblasts failed to form myotubes. Dantrolene
and thapsigargin, which decrease intracellular calcium by different mechanisms, also inhibited differentiation. In addition, nifedipine and
verapamil inhibited the expression of myosin heavy chain and myogenin,
two markers of skeletal myoblast differentiation. In contrast, levels
of the transcriptional factor Myf5, which is expressed in
undifferentiated myoblasts, did not decline. Calcium channel blockade
also prevented the expression of a reporter driven by the skeletal
muscle
Reduction in Intracellular Calcium Levels
Inhibits Myoblast Differentiation*
§,, and
Cardiology and ¶ Endocrinology, Yale University
School of Medicine, New Haven, Connecticut 06520
-actin promoter. These data demonstrate that lowering
intracellular calcium levels inhibits the differentiation of skeletal
myoblasts into mature myotubes.
*
This work was supported in part by National
Institutes of Health Grant HL58442 (to S. R.).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.
Donaghue Medical Research Foundation Investigator.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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