Publication: The peculiar apoptotic behavior of skeletal muscle cells
Authors
Salucci, Sara ; Burattini, Sabrina ; Baldassarri, Valentina
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Publisher
F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Apoptosis plays an active role in maintaining
skeletal muscle homeostasis. Its deregulation is involved
in several skeletal muscle disorders such as dystrophies,
myopathies, disuse and sarcopenia.
The aim of this work was to study in vitro the
apoptotic behavior induced by etoposide, staurosporine
and hydrogen peroxide in the C2C12 skeletal muscle cell
line, comparing myoblast vs myotube sensitivity,
investigated by means of morphological and
cytofluorimetric analyses.
Myotubes appeared more resistant than myoblasts to
apoptotic induction. In myoblasts treated with etoposide,
nuclei with chromatin condensation were observed, in
the presence of a diffuse DNA fragmentation, as shown
by confocal microscopy. The latter also appeared in
myotubes, where apoptotic and normal nuclei coexisted
inside the same syncytium. After staurosporine
treatment, myobalsts evidenced late apoptotic features
and a high number of TUNEL-positive nuclei.
Secondary necrosis appeared in myotubes, where
myonuclei with cleaved DNA again coexisted with
normal myonuclei. After H2O2 exposure, myotubes,
differently from myoblasts, showed a poor sensitivity to
cell death. Intriguingly, autophagic granules appeared
abundantly in myotubes after each treatment. In
myotubes, mitochondria were better preserved than in
myoblasts since those which were damaged were
probably degraded through autophagic processes. These findings demonstrate a scarce sensitivity of
myotubes to apoptotic stimuli due to acquisition of an
apoptosis-resistant phenotype during differentiation. The
presence of nuclear-dependent “territorial” death
domains in the syncytium could explain a slower death
of myotubes compared to mononucleated cells. In
addition, autophagy could preserve and protect muscle cell integrity against chemical stimuli, making C2C12
cells, in particular myotubes, more resistant to apoptosis
induction.
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