Modulation of Brain Hemichannels and Gap Junction Channels by Pro-Inflammatory Agents and Their Possible Role in Neurodegeneration

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dc.catalogadorpva
dc.contributor.authorOrellana Roca, Juan Andrés
dc.contributor.authorSáez Pedraza, Pablo José
dc.contributor.authorShoji Sánchez, Kenji Fabricio
dc.contributor.authorSchalper Casanova, Kurt Alex
dc.contributor.authorPalacios Prado, Nicolás
dc.contributor.authorVelarde Aliaga, María Victoria
dc.contributor.authorGiaume, Christian
dc.contributor.authorBennett, Michael V. L.
dc.contributor.authorSáez, Juan Carlos
dc.date.accessioned2024-10-15T19:48:41Z
dc.date.available2024-10-15T19:48:41Z
dc.date.issued2009
dc.description.abstractIn normal brain, neurons, astrocytes, and oligodendrocytes, the most abundant and active cells express pannexins and connexins, protein subunits of two families forming membrane channels. Most available evidence indicates that in mammals endogenously expressed pannexins form only hemichannels and connexins form both gap junction channels and hemichannels. Whereas gap junction channels connect the cytoplasm of contacting cells and coordinate electric and metabolic activity, hemichannels communicate the intra-and extracellular compartments and serve as a diffusional pathway for ions and small molecules. A subthreshold stimulation by acute pathological threatening conditions (e. g., global ischemia subthreshold for cell death) enhances neuronal Cx36 and glial Cx43 hemichannel activity, favoring ATP release and generation of preconditioning. If the stimulus is sufficiently deleterious, microglia become overactivated and release bioactive molecules that increase the activity of hemichannels and reduce gap junctional communication in astroglial networks, depriving neurons of astrocytic protective functions, and further reducing neuronal viability. Continuous glial activation triggered by low levels of anomalous proteins expressed in several neurodegenerative diseases induce glial hemichannel and gap junction channel disorders similar to those of acute inflammatory responses triggered by ischemia or infectious diseases. These changes are likely to occur in diverse cell types of the CNS and contribute to neurodegeneration during inflammatory process. Antiox. Redox Signal. 11, 369-399.
dc.description.funderFONDECYT
dc.fuente.origenHistorial Académico
dc.identifier.doi10.1089/ars.2008.2130
dc.identifier.eissn1557-7716
dc.identifier.issn1523-0864
dc.identifier.pubmedidPMID: 18816186
dc.identifier.urihttps://doi.org/10.1089/ars.2008.2130
dc.identifier.urihttps://publons.com/wos-op/publon/4315359/
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/88239
dc.identifier.wosidWOS:000261863200015
dc.information.autorucEscuela de Medicina; Orellana Roca, Juan Andrés; 0000-0003-4076-207X; 126007
dc.information.autorucFacultad de Ciencias Biológicas; Sáez Pedraza, Pablo José; 0000-0003-0521-9426; 132607
dc.information.autorucFacultad de Ciencias Biológicas; Shoji Sánchez, Kenji Fabricio; S/I; 134136
dc.information.autorucEscuela de Medicina; Schalper Casanova, Kurt Alex; S/I; 151783
dc.information.autorucFacultad de Ciencias Biológicas; Palacios Prado, Nicolás; S/I; 124928
dc.information.autorucFacultad de Ciencias Biológicas; Velarde Aliaga, María Victoria; S/I; 55362
dc.information.autorucFacultad de Ciencias Biológicas; Sáez, Juan Carlos; 0000-0003-3811-0347; 99913
dc.issue.numero2
dc.language.isoen
dc.nota.accesocontenido parcial
dc.pagina.final399
dc.pagina.inicio369
dc.publisherMary Ann Liebert
dc.revistaAntioxidants & Redox Signaling
dc.rightsacceso restringido
dc.subjectCENTRAL-NERVOUS-SYSTEM
dc.subjectNITRIC-OXIDE SYNTHASE
dc.subjectACTIVATED PROTEIN-KINASE
dc.subjectMICROGLIA-MEDIATED NEUROTOXICITY
dc.subjectCALCIUM-WAVE-PROPAGATION
dc.subjectFIBROBLAST-GROWTH-FACTOR
dc.subjectBETA-AMYLOID PEPTIDES
dc.subjectINTERCELLULAR COMMUNICATION
dc.subjectALPHA-SYNUCLEIN
dc.subjectATP RELEASE
dc.subject.ddc570
dc.subject.deweyBiologíaes_ES
dc.subject.ods03 Good health and well-being
dc.subject.odspa03 Salud y bienestar
dc.titleModulation of Brain Hemichannels and Gap Junction Channels by Pro-Inflammatory Agents and Their Possible Role in Neurodegeneration
dc.typeartículo
dc.volumen11
sipa.codpersvinculados126007
sipa.codpersvinculados132607
sipa.codpersvinculados134136
sipa.codpersvinculados151783
sipa.codpersvinculados124928
sipa.codpersvinculados55362
sipa.codpersvinculados99913
sipa.trazabilidadHistorial Académico;09-07-2021
sipa.trazabilidadORCID;2024-10-14
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