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17β‐Estradiol Abrogates Apoptosis Inhibiting PKCδ, JNK, and p66Shc Activation in C2C12 Cells
Author(s) -
La Colla Anabela,
Boland Ricardo,
Vasconsuelo Andrea
Publication year - 2015
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.25107
Subject(s) - microbiology and biotechnology , skeletal muscle , c2c12 , apoptosis , mitochondrion , phosphorylation , signal transduction , protein kinase c , chemistry , myocyte , oxidative stress , biology , endocrinology , biochemistry , myogenesis
Abstract 17β‐Estradiol (E2) protects several non‐reproductive tissues from apoptosis, including skeletal muscle. Previously, we showed that E2 at physiological concentrations prevented apoptosis induced by H 2 O 2 in skeletal myoblasts. As we have also demonstrated a clear beneficial action of this hormone on skeletal muscle mitochondria, the present work further characterizes the signaling mechanisms modulated by E2 that are involved in mitochondria protection, which ultimately result in antiapoptosis. Here, we report that E2 through estrogen receptors (ERs) inhibited the H 2 O 2 ‐induced PKCδ and JNK activation, which results in the inhibition of phosphorylation and translocation to mitochondria of the adaptor protein p66Shc. In conjunction, the inhibition by the hormone of this H 2 O 2 ‐triggered signaling pathway results in protection of mitochondrial potential membrane. Our results provide basis for a putative mechanism by which E2 exerts beneficial effects on mitochondria, against oxidative stress, in skeletal muscle cells. J. Cell. Biochem. 116: 1454–1465, 2015. © 2015 Wiley Periodicals, Inc.