TRPV1-Estradiol Stereospecific Relationship Underlies Cell Survival in Oxidative Cell Death

Ricardo Ramírez-Barrantes, Karina Carvajal-Zamorano, Belen Rodriguez, Claudio Cordova, Carlo Lozano, Felipe Simon, Paula Díaz, Pablo Muñoz, Ivanny Marchant, Ramón Latorre, Karen Castillo, Pablo Olivero

Resultado de la investigación: Contribución a una revistaArtículorevisión exhaustiva

4 Citas (Scopus)

Resumen

17β-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 17β-estradiol to enhance metabolic performance in injured cells. Specifically, in TRPV1 expressing cells, the application of 17β-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, 17β-estradiol potentiates TRPV1 single channel activity associated with an increased open probability. This effect was not observed after the application of 17α-estradiol. We explored the TRPV1-Estrogen relationship also in primary culture of hippocampal-derived neurons and observed that 17β-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 17β-estradiol-activated ionotropic membrane receptor coupling with mitochondrial function and cell survival.

Idioma originalInglés
Número de artículo444
PublicaciónFrontiers in Physiology
Volumen11
DOI
EstadoPublicada - 26 may. 2020

Áreas temáticas de ASJC Scopus

  • Fisiología
  • Fisiología (médica)

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