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Vol. 11, Issue 5, 1859-1874, May 2000
Department of Human Anatomy and Cell Science, University of
Manitoba, Winnipeg, Manitoba, Canada R3E 0W3
Muscle satellite cells are quiescent precursors interposed between
myofibers and a sheath of external lamina. Although their activation
and recruitment to cycle enable muscle repair and adaptation, the
activation signal is not known. Evidence is presented that nitric oxide
(NO) mediates satellite cell activation, including morphological
hypertrophy and decreased adhesion in the fiber-lamina complex.
Activation in vivo occurred within 1 min after injury. Cell isolation
and histology showed that pharmacological inhibition of nitric oxide
synthase (NOS) activity prevented the immediate injury-induced myogenic
cell release and delayed the hypertrophy of satellite cells in that
muscle. Transient activation of satellite cells in contralateral
muscles 10 min later suggested that a circulating factor may interact
with NO-mediated signaling. Interestingly, satellite cell activation in
muscles of mdx dystrophic mice and NOS-I knockout mice
quantitatively resembled NOS-inhibited release of normal cells, in
agreement with reports of displaced and reduced NOS expression in
dystrophin-deficient mdx muscle and the complete loss
of NOS-I expression in knockout mice. Brief NOS inhibition in normal
and mdx mice during injury produced subtle alterations in
subsequent repair, including apoptosis in myotube nuclei and myotube
formation inside laminar sheaths. Longer NOS inhibition delayed and
restricted the extent of repair and resulted in fiber branching. A
model proposes the hypothesis that NO release mediates satellite cell
activation, possibly via shear-induced rapid increases in NOS activity
that produce "NO transients."
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