期刊
FRONTIERS IN PHYSIOLOGY
卷 11, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fphys.2020.00444
关键词
TRPV1; 17 beta-estradiol; cell death; membrane receptor; neuroprotection
类别
资金
- Fondo Nacional de Desarrollo Cientifico y Tecnologico: Fondecyt [Fondecyt 11100047, DIUV 21, ACT-1104, Fondecyt 1121078, FONDECYT 1180999, FONDECYT 1190203]
- Iniciativa Cientifica Milenio of the Ministry of Economy, Development and Tourism (Chile)
- Millennium Scientific Initiative of the Chilean Ministry of Economy, Development, and Tourism [P029-022-F]
17 beta-estradiol is a neuronal survival factor against oxidative stress that triggers its protective effect even in the absence of classical estrogen receptors. The polymodal transient receptor potential vanilloid subtype 1 (TRPV1) channel has been proposed as a steroid receptor implied in tissue protection against oxidative damage. We show here that TRPV1 is sufficient condition for 17 beta-estradiol to enhance metabolic performance in injured cells. Specifically, in TRPV1 expressing cells, the application of 17 beta-estradiol within the first 3 h avoided H2O2-dependent mitochondrial depolarization and the activation of caspase 3/7 protecting against the irreversible damage triggered by H2O2. Furthermore, 17 beta-estradiol potentiates TRPV1 single channel activity associated with an increased open probability. This effect was not observed after the application of 17 alpha-estradiol. We explored the TRPV1-Estrogen relationship also in primary culture of hippocampal-derived neurons and observed that 17 beta-estradiol cell protection against H2O2-induced damage was independent of estrogen receptors pathway activation, membrane started and stereospecific. These results support the role of TRPV1 as a 17 beta-estradiol-activated ionotropic membrane receptor coupling with mitochondrial function and cell survival.
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