 |
 Previous Article | Next Article 
Journal of Neuroscience, Vol 9, 3443-3453, Copyright © 1989 by Society for Neuroscience
Ca2+ and Na+ currents in developing skeletal myoblasts are expressed in a sequential program: reversible suppression by transforming growth factor beta-1, an inhibitor of the myogenic pathway
JM Caffrey, AM Brown and MD Schneider
Department of Physiology and Molecular Biophysics, Baylor College of Medicine, Houston, Texas 77030.
We have analyzed the biophysical and developmental properties of Ca2+ and
Na+ currents in C2 muscle cells, whose morphological and biochemical
phenotype closely resembles differentiated skeletal muscle. Both fused and
unfused C2 myocytes possessed: (1) membrane capacitance consistent with the
presence of complex sarcotubular invaginations, (2) tetrodotoxin-sensitive
Na+ channels, and (3) "fast" and "slow" Ca2+ channels that inactivated at
holding potentials of -40 and -20 mV, respectively. Thus, the passive
electrical properties, Na+ currents, and Ca2+ currents expressed in C2
cells each differed from those found in the nonfusing muscle cell line,
BC3H1, and corresponded more precisely to characteristic findings observed
in skeletal muscle fibers. In further contrast to BC3H1 cells, C2 muscle
also expressed "transient" Ca2+ channels similar to those reported in
embryonic or neonatal skeletal muscle, which were detected within 12-24 hr
of mitogen withdrawal, up to 60 hr before appearance of "fast" and "slow"
currents. Na+ channels also were induced 12-24 hr after mitogen withdrawal.
Unlike the "fast" and "slow" Ca2+ currents, which were maximally expressed
at 8-14 d of serum withdrawal, "transient" Ca2+ channels became
down-regulated upon prolonged differentiation (as found in postnatal
skeletal muscle in vivo) and were no longer expressed at 14 d. Despite
their divergent kinetic and developmental properties, all components of
Ca2+ and Na+ current in C2 myocytes were suppressed reversibly in the
presence of transforming growth factor beta-1, a purified growth factor
that inhibits the myogenic phenotype. The results indicate that fusion is
not essential for skeletal myoblasts to produce developmentally regulated
voltage-gated channels that resemble those of intact muscle and demonstrate
that the formation of diverse Ca2+ and Na+ channels can be mediated by a
single peptide that affects the myogenic pathway.
This article has been cited by other articles:
|
|
|
|
 
E. Zebedin, M. Mille, M. Speiser, T. Zarrabi, W. Sandtner, B. Latzenhofer, H. Todt, and K. Hilber
C2C12 skeletal muscle cells adopt cardiac-like sodium current properties in a cardiac cell environment
Am J Physiol Heart Circ Physiol,
January 1, 2007;
292(1):
H439 - H450.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
F. Grassi, F. Pagani, G. Spinelli, L. De Angelis, G. Cossu, and F. Eusebi
Fusion-independent expression of functional ACh receptors in mouse mesoangioblast stem cells contacting muscle cells
J. Physiol.,
October 15, 2004;
560(2):
479 - 489.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
L. Mejia-Luna and G. Avila
Ca2+ channel regulation by transforming growth factor-{beta}1 and bone morphogenetic protein-2 in developing mice myotubes
J. Physiol.,
August 15, 2004;
559(1):
41 - 54.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
H. C. Ott, S. Berjukow, R. Marksteiner, E. Margreiter, G. Bock, G. Laufer, and S. Hering
On the fate of skeletal myoblasts in a cardiac environment: down-regulation of voltage-gated ion channels
J. Physiol.,
August 1, 2004;
558(3):
793 - 805.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
E. Zebedin, W. Sandtner, S. Galler, J. Szendroedi, H. Just, H. Todt, and K. Hilber
Fiber type conversion alters inactivation of voltage-dependent sodium currents in murine C2C12 skeletal muscle cells
Am J Physiol Cell Physiol,
August 1, 2004;
287(2):
C270 - C280.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
C Cognard, B Constantin, M Rivet-Bastide, N Imbert, C Besse, and G Raymond
Appearance and evolution of calcium currents and contraction during the early post-fusional stages of rat skeletal muscle cells developing in primary culture
Development,
January 3, 1993;
117(3):
1153 - 1161.
[Abstract]
[PDF]
|
|
|
|
