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17β‐Estradiol Protects Skeletal Myoblasts From Apoptosis Through p53, Bcl‐2, and FoxO Families
Author(s) -
La Colla Anabela,
Vasconsuelo Andrea,
Milanesi Lorena,
Pronsato Lucía
Publication year - 2017
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.25616
Subject(s) - c2c12 , skeletal muscle , apoptosis , transcription factor , microbiology and biotechnology , myocyte , transcription (linguistics) , biology , mdm2 , puma , gene , chemistry , myogenesis , endocrinology , genetics , linguistics , philosophy
ABSTRACT 17β‐Estradiol (E 2 ) protects several nonreproductive tissues from apoptosis, including skeletal muscle. Previously, we showed that E 2 at physiological concentrations prevented apoptosis induced by H 2 O 2 in skeletal myoblasts, reverting PKCδ, JNK, and p66Shc activation and exerting a beneficial action over mitochondria. Since genomic actions underlying the regulation of nuclear gene transcription are a common property of this steroid, the present work characterizes the transcriptional activity modulated by E 2 to exert its antiapoptotic effect. We report that E 2 protects skeletal myoblasts against apoptosis induced by H 2 O 2 modulating p53 and FoxO transcription factors and then their target genes Bcl‐2, Bim, Puma, PERP, and MDM2, without affecting Noxa gene. The results presented in this work support the notion that the transcription factors FoxO and p53 coordinate apoptosis in C2C12 cells, and deepens our knowledge about a putative molecular mechanism by which E 2 exerts beneficial effects against oxidative stress in skeletal myoblasts. J. Cell. Biochem. 118: 104–115, 2017. © 2016 Wiley Periodicals, Inc.