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dc.contributor.authorGajardo-Gómez R.
dc.contributor.authorSantibañez C.A.
dc.contributor.authorLabra V.C.
dc.contributor.authorGómez G.I.
dc.contributor.authorEugenin E.A.
dc.contributor.authorOrellana J.A.
dc.date.accessioned2020-09-02T22:18:18Z
dc.date.available2020-09-02T22:18:18Z
dc.date.issued2020
dc.identifier10.3390/ijms21072503
dc.identifier.citation21, 7, -
dc.identifier.issn16616596
dc.identifier.urihttps://hdl.handle.net/20.500.12728/4564
dc.descriptionAt least half of human immunodeficiency virus (HIV)-infected individuals suffer from a wide range of cognitive, behavioral and motor deficits, collectively known as HIV-associated neurocognitive disorders (HAND). The molecular mechanisms that amplify damage within the brain of HIV-infected individuals are unknown. Recently, we described that HIV augments the opening of connexin-43 (Cx43) hemichannels in cultured human astrocytes, which result in the collapse of neuronal processes. Whether HIV soluble viral proteins such as gp120, can regulate hemichannel opening in astrocytes is still ignored. These channels communicate the cytosol with the extracellular space during pathological conditions. We found that gp120 enhances the function of both Cx43 hemichannels and pannexin-1 channels in mouse cortical astrocytes. These effects depended on the activation of IL-1β/TNF-α, p38 MAP kinase, iNOS, cytoplasmic Ca2+ and purinergic signaling. The gp120-induced channel opening resulted in alterations in Ca2+ dynamics, nitric oxide production and ATP release. Although the channel opening evoked by gp120 in astrocytes was reproduced in ex vivo brain preparations, these responses were heterogeneous depending on the CA1 region analyzed. We speculate that soluble gp120-induced activation of astroglial Cx43 hemichannels and pannexin-1 channels could be crucial for the pathogenesis of HAND. © 2020 by the authors. Licensee MDPI, Basel, Switzerland.
dc.language.isoen
dc.publisherMDPI AG
dc.subjectAstrocyte
dc.subjectConnexins
dc.subjectCx43 hemichannels
dc.subjectGlia
dc.subjectGp120
dc.subjectHIV
dc.subjectcation channel
dc.subjectconnexin 43
dc.subjectglycoprotein gp 120
dc.subjectinterleukin 1beta
dc.subjectmitogen activated protein kinase
dc.subjectmitogen activated protein kinase p38
dc.subjectnitric oxide
dc.subjectpannexin 1 channel
dc.subjectprobenecid
dc.subjecttumor necrosis factor
dc.subjectunclassified drug
dc.subjectanimal cell
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectArticle
dc.subjectastrocyte
dc.subjectcell body
dc.subjectcell culture
dc.subjectconfocal microscopy
dc.subjectcontrolled study
dc.subjecthippocampus
dc.subjectHIV associated dementia
dc.subjecthuman
dc.subjecthuman cell
dc.subjectHuman immunodeficiency virus infection
dc.subjectimmunofluorescence test
dc.subjectincidence
dc.subjectmacroglia
dc.subjectmale
dc.subjectmouse
dc.subjectnerve function
dc.subjectneuropathology
dc.subjectnonhuman
dc.subjectprotein expression
dc.subjecttime lapse imaging
dc.titleHIV GP120 protein increases the function of connexin 43 hemichannels and pannexin-1 channels in astrocytes: Repercussions on astroglial function
dc.typeArticle


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