Apoptosis in differentiating C2C12 muscle cells selectively targets Bcl-2-deficient myotubes

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Issue Date
2014-01Author
Schöneich, Christian
Dremina, Elena S.
Galeva, Nadezhda A.
Sharov, Victor S.
Publisher
Springer Verlag
Type
Article
Article Version
Scholarly/refereed, author accepted manuscript
Rights
© Springer Science+Business Media New York 2013
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Show full item recordAbstract
Muscle cell apoptosis accompanies normal muscle development and regeneration, as well as
degenerative diseases and aging. C2C12 murine myoblast cells represent a common model to
study muscle differentiation. Though it was already shown that myogenic differentiation of C2C12
cells is accompanied by enhanced apoptosis in a fraction of cells, either the cell population
sensitive to apoptosis or regulatory mechanisms for the apoptotic response are unclear so far. In
the current study we characterize apoptotic phenotypes of different types of C2C12 cells at all
stages of differentiation, and report here that myotubes of differentiated C2C12 cells with low
levels of anti-apoptotic Bcl-2 expression are particularly vulnerable to apoptosis even though they
are displaying low levels of pro-apoptotic proteins Bax, Bak and Bad. In contrast, reserve cells
exhibit higher levels of Bcl-2 and high resistance to apoptosis. The transfection of proliferating
myoblasts with Bcl-2 prior to differentiation did not protect against spontaneous apoptosis
accompanying differentiation of C2C12 cell but led to Bcl-2 overexpression in myotubes and to
significant protection from apoptotic cell loss caused by exposure to hydrogen peroxide. Overall,
our data advocate for a Bcl-2-dependent mechanism of apoptosis in differentiated muscle cells.
However, downstream processes for spontaneous and hydrogen peroxide induced apoptosis are
not completely similar. Apoptosis in differentiating myoblasts and myotubes is regulated not
through interaction of Bcl-2 with pro-apoptotic Bcl-2 family proteins such as Bax, Bak, and Bad.
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Citation
Schöneich, C., Dremina, E., Galeva, N. et al. Apoptosis (2014) 19: 42. doi:10.1007/s10495-013-0922-7
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