Proinflammatory stimuli are needed for induction of microglial cell-mediated A beta PP244-C and A beta-neurotoxicity in hippocampal cultures

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dc.contributor.authorRamirez, Gigliola
dc.contributor.authorRey, Sergio
dc.contributor.authorvon Bernhardi, Rommy
dc.date.accessioned2024-01-10T13:52:35Z
dc.date.available2024-01-10T13:52:35Z
dc.date.issued2008
dc.description.abstractAmyloid-beta plaques and neurodegeneration are hallmarks of Alzheimer's disease, where glial cells are responsible for sustained neuroinflammation. Here we show that hippocampal-microglia co-cultures exposed to proinflammatory mediators, amyloid-beta- and amyloid-beta protein precursor construct-conjugated beads increased their production of nitrites. In contrast, inflammation was unable to significantly induce cell death by itself, whereas inflammation plus amyloid-beta or amyloid-beta protein precursor induced a significant increment of cell death and a 6-fold increase of production of Interleukin 1 beta. Those effects were not observed in the absence of microglia or when hippocampal cells were co-cultured with microglia for one day. In contrast, a 2-fold increase of transforming growth factor beta 1 was observed in hippocampal cultures exposed to inflammatory stimuli for 4 days, whereas induction of transforming growth factor beta 1 by inflammation plus amyloid-beta and amyloid-beta protein precursor was nearly abolished by microglia. Our results indicate that neurotoxicity induced by amyloid-beta or amyloid-beta protein precursor was a slow process depending on activated microglia and additional stimuli. The observed cytotoxicity could be consequence of a vicious cycle in which elevated concentrations of Interleukin 1 beta and radical species along with decreased secretion of neuroprotective cytokines such as transforming growth factor beta 1 support persistent activation of glial cells and cell damage.
dc.description.funderFONDECYT
dc.format.extent15 páginas
dc.fuente.origenWOS
dc.identifier.eissn1875-8908
dc.identifier.issn1387-2877
dc.identifier.pubmedidMEDLINE:18780966
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/79673
dc.identifier.wosidWOS:000258878800004
dc.information.autorucMedicina;Ramírez G;S/I;1001936
dc.information.autorucMedicina;Rey S;S/I;1083
dc.information.autorucMedicina;Von Bernhardi R;S/I;62523
dc.issue.numero1
dc.language.isoen
dc.nota.accesoSin adjunto
dc.pagina.final59
dc.pagina.inicio45
dc.publisherIOS PRESS
dc.revistaJOURNAL OF ALZHEIMERS DISEASE
dc.rightsregistro bibliográfico
dc.subjectAlzheimer's disease
dc.subjectcell death
dc.subjectcytokines
dc.subjectglial cells
dc.subjectneurodegenerative disease
dc.subjectneuroinflammation
dc.subjectAMYLOID PRECURSOR PROTEIN
dc.subjectALZHEIMERS-DISEASE
dc.subjectNITRIC-OXIDE
dc.subjectIN-VITRO
dc.subjectOXIDATIVE STRESS
dc.subjectSENILE PLAQUES
dc.subjectINTERLEUKIN-1
dc.subjectINFLAMMATION
dc.subjectIDENTIFICATION
dc.subjectMETABOLISM
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleProinflammatory stimuli are needed for induction of microglial cell-mediated A beta PP244-C and A beta-neurotoxicity in hippocampal cultures
dc.typeartículo
dc.volumen15
sipa.codpersvinculados1001936
sipa.codpersvinculados1083
sipa.codpersvinculados62523
sipa.indexWOS
sipa.indexScopus
sipa.trazabilidadCarga SIPA;09-01-2024
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