Disruption in connexin-based communication is associated with intracellular Ca²⁺ signal alterations in astrocytes from Niemann-Pick type C mice

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dc.catalogadoryvc
dc.contributor.authorSáez Pedraza, Pablo José
dc.contributor.authorOrellana Roca, Juan Andrés
dc.contributor.authorVega-Riveros, Natalia
dc.contributor.authorFigueroa, Vania A.
dc.contributor.authorHernández Trejo, Diego Eduardo
dc.contributor.authorCastro, Juan Francisco
dc.contributor.authorKlein Posternack, Andrés David
dc.contributor.authorJean X. Jiang
dc.contributor.authorZanlungo Matsuhiro, Silvana
dc.contributor.authorSáez Carreño, Juan Carlos
dc.date.accessioned2024-06-06T19:19:45Z
dc.date.available2024-06-06T19:19:45Z
dc.date.issued2013
dc.description.abstractReduced astrocytic gap junctional communication and enhanced hemichannel activity were recently shown to increase astroglial and neuronal vulnerability to neuroinflammation. Moreover, increasing evidence suggests that neuroinflammation plays a pivotal role in the development of Niemann-Pick type C (NPC) disease, an autosomal lethal neurodegenerative disorder that is mainly caused by mutations in the NPC1 gene. Therefore, we investigated whether the lack of NPC1 expression in murine astrocytes affects the functional state of gap junction channels and hemichannels. Cultured cortical astrocytes of NPC1 knock-out mice (Npc1⁻/⁻) showed reduced intercellular communication via gap junctions and increased hemichannel activity. Similarly, astrocytes of newborn Npc1⁻/⁻ hippocampal slices presented high hemichannel activity, which was completely abrogated by connexin 43 hemichannel blockers and was resistant to inhibitors of pannexin 1 hemichannels. Npc1⁻/⁻ astrocytes also showed more intracellular Ca²⁺ signal oscillations mediated by functional connexin 43 hemichannels and P2Y₁ receptors. Therefore, Npc1⁻/⁻ astrocytes present features of connexin based channels compatible with those of reactive astrocytes and hemichannels might be a novel therapeutic target to reduce neuroinflammation in NPC disease.
dc.fuente.origenORCID
dc.identifier.doi10.1371/journal.pone.0071361
dc.identifier.urihttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23977027/?tool=EBI
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/86573
dc.information.autorucFacultad de Ciencias Biológicas;Sáez Pedraza, Pablo José;0000-0003-0521-9426;132607
dc.information.autorucEscuela de Medicina;Orellana Roca, Juan Andrés 0000-0003-4076-207X;126007
dc.information.autorucFacultad de Ciencias Biológicas;Vega-Riveros, Natalia;S/I;142379
dc.information.autorucFacultad de Ciencias Biológicas;Hernández Trejo, Diego Eduardo;S/I;142368
dc.information.autorucFacultad de Ciencias Biológicas;Klein Posternack, Andrés David;S/I;2966
dc.information.autorucEscuela de Medicina; Zanlungo Matsuhiro, Silvana; 0000-0001-8383-9829; 72650
dc.information.autorucFacultad de Ciencias Biológicas;Sáez Carreño, Juan Carlos;0000-0003-3811-0347;99913
dc.language.isoen
dc.nota.accesocontenido completo
dc.rightsacceso abierto
dc.subject.ddc610
dc.subject.deweyMedicina y saludes_ES
dc.titleDisruption in connexin-based communication is associated with intracellular Ca²⁺ signal alterations in astrocytes from Niemann-Pick type C mice
dc.typeartículo
sipa.codpersvinculados72650
sipa.trazabilidadORCID;2024-06-03
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