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Glucose deprivation induces reticulum stress by the PERK pathway and caspase-7- and calpain-mediated caspase-12 activation

dc.creatorDe la Cadena, Selene Garcia
dc.creatorHernandez-Fonseca, Karla
dc.creatorMassieu, Lourdes
dc.date.accessioned2017-06-29T03:51:39Z
dc.date.available2017-06-29T03:51:39Z
dc.date.issued2014es_ES
dc.identifier2739es_ES
dc.identifier.issn1360-8185es_ES
dc.identifier.urihttp://repositorio.inprf.gob.mx/handle/123456789/4588
dc.identifier.urihttps://doi.org/10.1007/s10495-013-0930-7es_ES
dc.language.isoenges_ES
dc.publisherDordrecht, Netherlands : Springeres_ES
dc.relation19 (3) 141-427 p.es_ES
dc.relationversión del editores_ES
dc.rightsacceso cerradoes_ES
dc.titleGlucose deprivation induces reticulum stress by the PERK pathway and caspase-7- and calpain-mediated caspase-12 activationes_ES
dc.typeartículoes_ES
dc.contributor.affiliationDivisión de Neurociencias, Departamento de Neuropatología Molecular, Instituto de Fisiología Celular, Universidad Nacional Autónoma de Méxicoes_ES
dc.relation.jnabreviadoAPOPTOSISes_ES
dc.relation.journalApoptosises_ES
dc.identifier.placePaíses Bajoses_ES
dc.date.published2014es_ES
dc.identifier.organizacionInstituto Nacional de Psiquiatría Ramón de la Fuente Muñizes_ES
dc.identifier.eissn1573-675Xes_ES
dc.identifier.doi10.1007/s10495-013-0930-7es_ES
dc.description.monthMares_ES
dc.description.abstractotrodiomaGlucose is the main energy source in brain and it is critical for correct brain functioning. Type 1 diabetic patients might suffer from severe hypoglycemia if exceeding insulin administration, which can lead to acute brain injury if not opportunely corrected. The mechanisms leading to hypoglycemic brain damage are not completely understood and the role of endoplasmic reticulum (ER) stress has not been studied. ER stress resulting from the accumulation of unfolded or misfolded proteins in the ER is counteracted by the unfolded protein response (UPR). When the UPR is sustained, apoptotic death might take place. We have examined UPR activation during glucose deprivation (GD) in hippocampal cultured neurons and its role in the induction of apoptosis. Activation of the PERK pathway of the UPR was observed, as increased phosphorylation of eIF2α and elevated levels of the transcription factor ATF4, occurred 30 min after GD and the levels of the chaperone protein, GRP78 and the transcription factor CHOP, increased after 2 h of GD. In addition, we observed an early activation of caspase-7 and 12 during GD, while caspase-3 activity increased only transiently during glucose reintroduction. Inhibition of caspase-3/7 and the calcium-dependent protease, calpain, significantly decreased caspase-12 activity. The ER stress inhibitor, salubrinal prevented neuronal death and caspase-12 activity. Results suggest that the PERK pathway of the UPR is involved in GD-induced apoptotic neuronal death through the activation of caspase-12, rather than the mitochondrial-dependent caspase pathway. In addition, we show that calpain and caspase-7 are soon activated after GD and mediate caspase-12 activation and neuronal death.es_ES


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