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CB2 cannabinoid receptors modulate HIF-1α and TIM-3 expression in a hypoxia-ischemia mouse model

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dc.contributor.author Kossatz, Elk
dc.contributor.author Maldonado, Rafael, 1961-
dc.contributor.author Robledo, Patricia, 1958-
dc.date.accessioned 2017-04-20T07:19:52Z
dc.date.issued 2016
dc.identifier.citation Kossatz E, Maldonado R, Robledo P. CB2 cannabinoid receptors modulate HIF-1α and TIM-3 expression in a hypoxia-ischemia mouse mode. Eur Neuropsychopharmacol. 2016 Dec;26(12):1972-88. DOI: 10.1016/j.euroneuro.2016.10.003
dc.identifier.issn 0924-977X
dc.identifier.uri http://hdl.handle.net/10230/30847
dc.description.abstract The role of CB2 cannabinoid receptors (CB2R) in global brain lesions induced by hypoxia-ischemia (HI) insult is still unresolved. The aim of this study was to evaluate the involvement of CB2R in the behavioural and biochemical underpinnings related to brain damage induced by HI in adult mice, and the mechanisms involved. CB2R knockout (KO) mice and wild-type littermates (WT) underwent permanent ligation of the left common carotid artery and hypoxia. Behavioural measurements in the rotarod, beam walking, object recognition, open field, and Irwin tests were carried out 24h, 72h and 7 days. In KO mice, more extensive brain injury was observed. Behavioural deficits in the Irwin test were observed in both genotypes; while WT mice showed progressive recovery by day 7, KO mice did not. Only KO mice showed alterations in motor learning, coordination and balance, and did not recover over time. A higher expression of microglia and astrocytes was observed in several brain areas of lesioned WT and KO mice. The possible alteration of the inflammatory-related factors HIF-1α and TIM-3 was evaluated in these animals. In both genotypes, HIF-1α and TIM-3 expression was observed in lesioned areas associated with activated microglia. However, the expression levels of these proteins were exacerbated in KO mice in several lesioned and non-lesioned brain structures. Our results indicate that CB2R may have a crucial neuroprotective role following HI insult through the modulation of the inflammatory-related HIF-1α/TIM-3 signalling pathway in microglia.
dc.description.sponsorship This work was supported by the European Commission, FP7 (#HEALTH-F2-2013-602891), the Spanish Ministerio de Economía y Competitividad-MINECO (#SAF2014-59648-P), the Spanish Instituto de Salud Carlos III, RETICS-RTA (#RD12/0028/0023) and the Generalitat de Catalunya, AGAUR (#2014-SGR-1547). C.L.P. and R.N. are recipients of a predoctoral fellowship from the Spanish Ministerio de Educación, Cultura y Deporte (MECD) and the Spanish MINECO, respectively. I.M.L.M. is a recipient of a predoctoral fellowship from the Mexican Consejo Nacional de Ciencia y Tecnología (CONACyT). FEDER partial funding is also acknowledged
dc.format.mimetype application/pdf
dc.language.iso eng
dc.publisher Elsevier
dc.relation.ispartof European Neuropsychopharmacology. 2016 Dec;26(12):1972-88
dc.rights © Elsevier http://dx.doi.org/10.1016/j.euroneuro.2016.10.003
dc.subject.other Cervell -- Ferides i lesions
dc.subject.other Isquèmia
dc.subject.other Anoxèmia
dc.subject.other Cannabinoides -- Receptors
dc.title CB2 cannabinoid receptors modulate HIF-1α and TIM-3 expression in a hypoxia-ischemia mouse model
dc.type info:eu-repo/semantics/article
dc.identifier.doi http://dx.doi.org/10.1016/j.euroneuro.2016.10.003
dc.relation.projectID info:eu-repo/grantAgreement/EC/FP7/602891
dc.relation.projectID info:eu-repo/grantAgreement/ES/1PE/SAF2014-59648-P
dc.rights.accessRights info:eu-repo/semantics/openAccess
dc.type.version info:eu-repo/semantics/acceptedVersion

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