Interferon-γ and high glucose-induced opening of Cx43 hemichannels causes endothelial cell dysfunction and damage

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dc.contributor.authorSáez, Juan C.
dc.contributor.authorContreras-Duarte, Susana
dc.contributor.authorLabra, Valeria C.
dc.contributor.authorSantibañez, Cristian A.
dc.contributor.authorMellado, Luis A.
dc.contributor.authorInostroza, Carla A.
dc.contributor.authorAlvear, Tanhia F.
dc.contributor.authorRetamal, Mauricio
dc.contributor.authorVelarde, Victoria
dc.contributor.authorOrellana, Juan A.
dc.date.accessioned2021-07-12T16:13:59Z
dc.date.available2021-07-12T16:13:59Z
dc.date.issued2020
dc.description.abstractBoth IFN-γ or high glucose have been linked to systemic inflammatory imbalance with serious repercussions not only for endothelial function but also for the formation of the atherosclerotic plaque. Although the uncontrolled opening of connexin hemichannels underpins the progression of various diseases, whether they are implicated in endothelial cell dysfunction and damage evoked by IFN-γ plus high glucose remains to be fully elucidated. In this study, by using live cell imaging and biochemical approaches, we demonstrate that IFN-γ plus high glucose augment endothelial connexin43 hemichannel activity, resulting in the increase of ATP release, ATP-mediated Ca2+ dynamics and production of nitric oxide and superoxide anion, as well as impaired insulin-mediated uptake and intercellular diffusion of glucose and cell survival. Based on our results, we propose that connexin 43 hemichannel inhibition could serve as a new approach for tackling the activation of detrimental signaling resulting in endothelial cell dysfunction and death caused by inflammatory mediators during atherosclerosis secondary to diabetes mellituses
dc.format.extent18 p.es
dc.identifier.citationBBA - Molecular Cell Research Volume 1867, Issue 8, August 2020, Article number 118720es
dc.identifier.urihttps://doi.org/10.1016/j.bbamcr.2020.118720es
dc.identifier.urihttp://hdl.handle.net/11447/4145
dc.language.isoenes
dc.subjectConnexonses
dc.subjectDiabeteses
dc.subjectEndotheliumes
dc.subjectHemichannelses
dc.subjectInflammationes
dc.titleInterferon-γ and high glucose-induced opening of Cx43 hemichannels causes endothelial cell dysfunction and damagees
dc.typeArticlees

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