HIV infection of astrocytes increases release of Dickkopf-1 protein by a gap junction and hemichannel dependent mechanism

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dc.article.numberP162
dc.catalogadorpva
dc.contributor.authorOrellana Roca, Juan Andrés
dc.contributor.authorSáez, Juan Carlos
dc.contributor.authorBerman, Joan
dc.contributor.authorEugenín Arce, Eliseo Alberto
dc.date.accessioned2024-10-15T19:13:55Z
dc.date.available2024-10-15T19:13:55Z
dc.date.issued2012
dc.description.abstractHuman immunodeficiency virus-1 (HIV) is a major public health issue, with a significant CNS complication of infection, NeuroAIDS. In vivo, microglia/macrophages are the main cells infected. However, a low but significant number of HIV infected astrocytes also has been detected, but their role in the pathogenesis of NeuroAIDS is not well understood. Our previous data indicated that HIV infection of astrocytes increased expression of the glycoprotein, dickkopf-1 protein (Dkk1), a soluble inhibitor of the wnt pathway. In HIV infected cultures of human astrocytes, secretion of Dkk1 was highly regulated by functional gap junction channels and connexin43 hemichannels. We also demonstrated that Dkk1 expression in astrocytes was increased in human brain tissue sections of individuals with HIV encephalitis as compared to tissue sections from uninfected individuals. We demonstrated that in primary cells, Dkk1 secretion did not participate in bystander killing of uninfected astrocytes or viral reactivation. However, its secretion regulates neuronal damage measured by collapse of neuronal processes. Thus, we demonstrated that HIV infection of astrocytes dysregulates secretion of Dkk1 by a mechanisms that involves both gap junctions as well as hemichannels that contributes to the neuropathogenesis observed in HIV infected individuals.
dc.fuente.origenConveris
dc.identifier.issn1355-0284
dc.identifier.scopusid000304487800163
dc.identifier.urihttps://publons.com/wos-op/publon/11458580/
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/88237
dc.identifier.wosidWOS:000304487800163
dc.information.autorucFacultad de Ciencias Biológicas; Orellana Roca, Juan Andrés; 0000-0003-4076-207X; 126007
dc.information.autorucFacultad de Ciencias Biológicas; Sáez, Juan Carlos; 0000-0003-3811-0347; 99913
dc.information.autorucFacultad de Ciencias Biológicas; Eugenín Arce, Eliseo Alberto; S/I; 6246
dc.issue.numeroSuppl. 1
dc.language.isoen
dc.nota.accesocontenido parcial
dc.pagina.final80
dc.pagina.inicio80
dc.publisherSpringer
dc.revistaJournal of Neurology
dc.rightsacceso restringido
dc.subjectNeurosciences
dc.subjectVirology
dc.subject.ddc610
dc.subject.deweyMedicina y saludes_ES
dc.subject.ods03 Good health and well-being
dc.subject.odspa03 Salud y bienestar
dc.titleHIV infection of astrocytes increases release of Dickkopf-1 protein by a gap junction and hemichannel dependent mechanism
dc.typeartículo
dc.volumen18
sipa.codpersvinculados126007
sipa.codpersvinculados99913
sipa.codpersvinculados6246
sipa.trazabilidadConveris;20-07-2021
sipa.trazabilidadORCID;2024-10-14
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