Examinando por Autor "Lozano, C."

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    Transient receptor potential vanilloid 1 expression mediates capsaicin-induced cell death
    (Frontiers Media S.A., 2018-06) Ramírez-Barrantes, R.; Córdova, C.; Gatica, S.; Rodriguez, B.; Lozano, C.; Marchant, I.; Echeverria, C.; Simon, F.; Olivero, P.
    The transient receptor potential (TRP) ion channel family consists of a broad variety of non-selective cation channels that integrate environmental physicochemical signals for dynamic homeostatic control. Involved in a variety of cellular physiological processes, TRP channels are fundamental to the control of the cell life cycle. TRP channels from the vanilloid (TRPV) family have been directly implicated in cell death. TRPV1 is activated by pain-inducing stimuli, including inflammatory endovanilloids and pungent exovanilloids, such as capsaicin (CAP). TRPV1 activation by high doses of CAP (> 10 μM) leads to necrosis, but also exhibits apoptotic characteristics. However, CAP dose-response studies are lacking in order to determine whether CAP-induced cell death occurs preferentially via necrosis or apoptosis. In addition, it is not known whether cytosolic Ca2+ and mitochondrial dysfunction participates in CAP-induced TRPV1-mediated cell death. By using TRPV1-transfected HeLa cells, we investigated the underlying mechanisms involved in CAP-induced TRPV1-mediated cell death, the dependence of CAP dose, and the participation of mitochondrial dysfunction and cytosolic Ca2+ increase. Together, our results contribute to elucidate the pathophysiological steps that follow after TRPV1 stimulation with CAP. Low concentrations of CAP (1 μM) induce cell death by a mechanism involving a TRPV1-mediated rapid and transient intracellular Ca2+ increase that stimulates plasma membrane depolarization, thereby compromising plasma membrane integrity and ultimately leading to cell death. Meanwhile, higher doses of CAP induce cell death via a TRPV1-independent mechanism, involving a slow and persistent intracellular Ca2+ increase that induces mitochondrial dysfunction, plasma membrane depolarization, plasma membrane loss of integrity, and ultimately, cell death. © 2018 Ramírez-Barrantes, Córdova, Gatica, Rodriguez, Lozano, Marchant, Echeverria, Simon and Olivero.
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    Ítem
    TRPV1-Estradiol Stereospecific Relationship Underlies Cell Survival in Oxidative Cell Death
    (Frontiers Media S.A., 2020-05) Ramírez Barrantes, R.; Carvajal Zamorano K., K.; Rodríguez, B.; Córdova, C.; Lozano, C.; Simón, F.; Díaz, P.; Muñoz, P.; Marchant, I.; Latorre, R.; Castillo, K.; Olivero, P.
    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. © Copyright © 2020 Ramírez-Barrantes, Carvajal-Zamorano, Rodriguez, Cordova, Lozano, Simon, Díaz, Muñoz, Marchant, Latorre, Castillo and Olivero.