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

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    Schoneich_Apoptosis_2014.pdf (4.174Mb)
    Issue Date
    2014-01
    Author
    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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    Abstract
    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.
    URI
    http://hdl.handle.net/1808/23604
    DOI
    https://doi.org/10.1007/s10495-013-0922-7
    Collections
    • Pharmaceutical Chemistry Scholarly Works [340]
    Citation
    Schöneich, C., Dremina, E., Galeva, N. et al. Apoptosis (2014) 19: 42. doi:10.1007/s10495-013-0922-7

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    Contact KU ScholarWorks
    785-864-8983
    KU Libraries
    1425 Jayhawk Blvd
    Lawrence, KS 66045
    785-864-8983

    KU Libraries
    1425 Jayhawk Blvd
    Lawrence, KS 66045
    Image Credits
     

     

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