Examinando por Autor "Encina, M."

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  • Miniatura
    Ítem
    A crowdsourcing-based system for monitoring em radiation exposure in Chile
    (CEUR-WS, 2018-10) Ulloa, J.J.; Encina, M.; Gutiérrez-Gaitán, M.; Ruete, D.; Gómez-Pantoja, C.
    Public concern about the possible effects on health due to electromagnetic (EM) radiation exposure has led to the definition of regulations worldwide. In Chile, the so-called "Ley de Antenas" provides a regulatory framework that establishes limits and special conditions in this regard. Although the official record of measurements is available in a public information portal, this approach is not scalable and intuitive enough for all interested users. This paper propose a participatory measurement system to extend the monitored areas based on the concern of citizens themselves. © 2018 CEUR-WS. All rights reserved.
  • Miniatura
    Ítem
    Prolonged AT1R activation induces CaV1.2 channel internalization in rat cardiomyocytes
    (Nature Publishing Group, 2017-12) Hermosilla, T.; Encina, M.; Morales, D.; Moreno, C.; Conejeros, C.; Alfaro-Valdés, H.M.; Lagos-Meza, F.; Simon, F.; Altier, C.; Varela, D.
    The cardiac L-type calcium channel is a multi-subunit complex that requires co-assembling of the pore-forming subunit CaV1.2 with auxiliary subunits CaVα2δ and CaVβ. Its traffic has been shown to be controlled by these subunits and by the activation of various G-protein coupled receptors (GPCR). Here, we explore the consequences of the prolonged activation of angiotensin receptor type 1 (AT1R) over CaV1.2 channel trafficking. Bioluminescence Resonance Energy Transfer (BRET) assay between β-arrestin and L-type channels in angiotensin II-stimulated cells was used to assess the functional consequence of AT1R activation, while immunofluorescence of adult rat cardiomyocytes revealed the effects of GPCR activation on CaV1.2 trafficking. Angiotensin II exposure results in β-arrestin1 recruitment to the channel complex and an apparent loss of CaV1.2 immunostaining at the T-tubules. Accordingly, angiotensin II stimulation causes a decrease in L-type current, Ca2+ transients and myocyte contractility, together with a faster repolarization phase of action potentials. Our results demonstrate that prolonged AT1R activation induces β-arrestin1 recruitment and the subsequent internalization of CaV1.2 channels with a half-dose of AngII on the order of 100 nM, suggesting that this effect depends on local renin-angiotensin system. This novel AT1R-dependent CaV1.2-trafficking modulation likely contributes to angiotensin II-mediated cardiac remodeling.