Estradiol exerts antiapoptotic effects in skeletal myoblasts via mitochondrial PTP and MnSOD

LA COLLA ANABELA; VASCONSUELO ANDREA; BOLAND RICARDO

JOURNAL OF ENDOCRINOLOGY

BIOSCIENTIFICA LTD

Lugar: Bristol; Año: 2013 p. 331 - 341

0022-0795

17b-Estradiol (E2) protects several non-reproductive tissues from apoptosis, includingskeletal muscle. We have shown that E2at physiological concentrations prevented apoptosisinduced by H2O2in C2C12 skeletal myoblasts. As we also demonstrated the presence ofestrogen receptors in mitochondria, the present workwas focused on the effects of E2on thisorganelle. Specifically, we evaluated the actions of E2on the mitochondrial permeabilitytransition pore (MPTP) by the calcein-acetoxymethylester/cobalt method using fluorescencemicroscopy and flow cytometry. Pretreatment with E2prevented MPTP opening induced byH2O2, which preceded loss of mitochondrial membrane potential. In addition, it wasobserved that H2O2induced translocation of Bax to mitochondria; however, in the presenceof the steroid this effect was abrogated suggesting that members of the Bcl-2 family may beregulated by E2to exert an antiapoptotic effect. Moreover, E2increased mitochondrialmanganese superoxide dismutase protein expression and activity, as part of a mechanismactivated by E2that improved mitochondrial performance. Our results suggest a role of E2inthe regulation of apoptosis with a clear action at the mitochondrial level in C2C12 skeletalmyoblast cells.