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dc.contributor.authorYstgaard, Martin Bogale
dc.contributor.authorScheffler, Katja
dc.contributor.authorSuganthan, Rajikala
dc.contributor.authorBjørås, Magnar
dc.contributor.authorRanheim, Trine
dc.contributor.authorSagen, Ellen Lund
dc.contributor.authorHalvorsen, Bente
dc.contributor.authorSaugstad, Ola Didrik
dc.contributor.authorYndestad, Arne
dc.date.accessioned2019-12-16T14:25:40Z
dc.date.available2019-12-16T14:25:40Z
dc.date.created2019-08-21T17:28:41Z
dc.date.issued2019
dc.identifier.citationNeonatology. 2019, 115 (4), 355-362.nb_NO
dc.identifier.issn1661-7800
dc.identifier.urihttp://hdl.handle.net/11250/2633465
dc.description.abstractBackground: Following birth asphyxia there is a robust inflammatory response. NLRP3 is a receptor of the innate immune system. Upon activation, NLRP3 forms an inflammasome together with ASC and procaspase-1 to mediate release of IL-1β and IL-18. NLRP3 has previously been shown to be upregulated following neonatal hypoxic-ischemic (HI) brain injury in mice, but with no early effect on brain injury. Objective: We aimed to evaluate if deficiency of NLRP3 or ASC protects against neonatal HI brain damage 7 days after hypoxia-ischemia. Methods: C57BL/6J, NLRP3–/–, and ASC–/– mice were subjected to unilateral common carotid artery ligation followed by hypoxia at P9. Brain infarction, apoptosis, and microglial response were evaluated, as well as total RNA sequencing and examination of plasma levels of systemic proinflammatory cytokines. Results: NLRP3–/– mice showed significantly increased brain infarction volumes compared to wild-type (Wt) mice, while ASC–/– mice showed reduced brain infarction volumes after neonatal hypoxia-ischemia. The amount of activated microglia was increased in NLRP3–/– mice, while decreased in ASC–/– mice compared to Wt mice. Total RNA sequencing showed an impaired inflammatory transcriptional response in the hippocampus of NLRP3–/– mice. Plasma levels of IL-1β and IL-18 were not affected, but TNF was lower in NLRP3–/– and ASC–/– mice compared to Wt mice. Conclusion: ASC deficiency is neuroprotective in neonatal HI brain damage in mice, while NLRP3 deficiency increases brain damage.nb_NO
dc.language.isoengnb_NO
dc.publisherKarger Publishersnb_NO
dc.titleNeuromodulatory effect of NLRP3 and ASC in neonatal hypoxic ischemic encephalopathynb_NO
dc.typeJournal articlenb_NO
dc.typePeer reviewednb_NO
dc.description.versionpublishedVersionnb_NO
dc.source.pagenumber355-362nb_NO
dc.source.volume115nb_NO
dc.source.journalNeonatologynb_NO
dc.source.issue4nb_NO
dc.identifier.doi10.1159/000497200
dc.identifier.cristin1717833
dc.description.localcodeThis article will not be available due to copyright restrictions (c) 2019 by Kargernb_NO
cristin.unitcode1920,0,0,0
cristin.unitcode194,65,15,0
cristin.unitnameSt. Olavs Hospital HF
cristin.unitnameInstitutt for klinisk og molekylær medisin
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1


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