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J Biol Chem, Vol. 274, Issue 42, 30315-30321, October 15, 1999
From the Caveolin-3 is the principal structural protein of
caveolae membrane domains in striated muscle cells. Caveolin-3 mRNA
and protein expression are dramatically induced during the
differentiation of C2C12 skeletal myoblasts, coincident with myoblast
fusion. In these myotubes, caveolin-3 localizes to the sarcolemma
(muscle cell plasma membrane), where it associates with the
dystrophin-glycoprotein complex. However, it remains unknown what role
caveolin-3 plays in myoblast differentiation and myotube formation.
Here, we employ an antisense approach to derive stable C2C12 myoblasts
that fail to express the caveolin-3 protein. We show that C2C12 cells
harboring caveolin-3 antisense undergo differentiation and express
normal amounts of four muscle-specific marker proteins. However, C2C12 cells harboring caveolin-3 antisense fail to undergo myoblast fusion
and, therefore, do not form myotubes. Interestingly, treatment with
specific p38 mitogen-activated protein kinase inhibitors blocks both
myotube formation and caveolin-3 expression, but does not affect the
expression of other muscle-specific proteins. In addition, we find that
three human rhabdomyosarcoma cell lines do not express caveolin-3 and
fail to undergo myoblast fusion. Taken together, these results support
the idea that caveolin-3 expression is required for myoblast fusion and
myotube formation, and suggest that p38 is an upstream regulator of
caveolin-3 expression.
Targeted Down-regulation of Caveolin-3 Is Sufficient to Inhibit
Myotube Formation in Differentiating C2C12 Myoblasts
TRANSIENT ACTIVATION OF p38 MITOGEN-ACTIVATED PROTEIN KINASE IS
REQUIRED FOR INDUCTION OF CAVEOLIN-3 EXPRESSION AND SUBSEQUENT MYOTUBE
FORMATION
,,,
Department of Molecular Pharmacology and
Albert Einstein Cancer Center and § Department of Cell
Biology and Albert Einstein Cancer Center, Albert Einstein College of
Medicine, Bronx, New York 10461
Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.
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