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

Research output: Contribution to journalArticlepeer-review

7 Citations (Scopus)


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.

Original languageEnglish
Article number444
JournalFrontiers in Physiology
Publication statusPublished - 26 May 2020


  • 17β-estradiol
  • cell death
  • membrane receptor
  • neuroprotection
  • TRPV1

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)


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