17β‐Estradiol Abrogates Apoptosis Inhibiting PKCδ, JNK, and p66Shc Activation in C2C12 Cells. Issue 7 (July 2015)

• Record Type: Journal Article
• Authors: La Colla, Anabela; Boland, Ricardo; Vasconsuelo, Andrea
• Is Part Of: Journal of cellular biochemistry. Volume 116:Issue 7(2015:Jul.)
• Page Start: 1454
• Page End: 1465
• Publication Date: 2015-07
• Subjects: Cytochemistry -- Periodicals; 572
• DOI: 10.1002/jcb.25107
• Languages: English
• ISSNs: 0730-2312

Abstract

<abstract abstract-type="main" xml:lang="en"> <title>Abstract</title> <sec id="jcb25107-sec-0001" sec-type="section"> <p>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 H₂O₂ 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 H₂O₂‐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 H₂O₂‐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.</p> </sec> </abstract>