000905217 001__ 905217
000905217 005__ 20230123110551.0
000905217 0247_ $$2doi$$a10.1007/s12975-021-00948-8
000905217 0247_ $$2ISSN$$a1868-4483
000905217 0247_ $$2ISSN$$a1868-601X
000905217 0247_ $$2Handle$$a2128/31253
000905217 0247_ $$2pmid$$a34628598
000905217 0247_ $$2WOS$$aWOS:000705686300001
000905217 037__ $$aFZJ-2022-00500
000905217 082__ $$a610
000905217 1001_ $$0P:(DE-HGF)0$$aHeinisch, Ole$$b0$$eCorresponding author
000905217 245__ $$aErythropoietin Abrogates Post-Ischemic Activation of the NLRP3, NLRC4, and AIM2 Inflammasomes in Microglia/Macrophages in a TAK1-Dependent Manner
000905217 260__ $$aNew York, NY$$bSpringer$$c2022
000905217 3367_ $$2DRIVER$$aarticle
000905217 3367_ $$2DataCite$$aOutput Types/Journal article
000905217 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1654252610_25140
000905217 3367_ $$2BibTeX$$aARTICLE
000905217 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000905217 3367_ $$00$$2EndNote$$aJournal Article
000905217 520__ $$aInflammasomes are known to contribute to brain damage after acute ischemic stroke (AIS). TAK1 is predominantly expressed in microglial cells and can regulate the NLRP3 inflammasome, but its impact on other inflammasomes including NLRC4 and AIM2 after AIS remains elusive. EPO has been shown to reduce NLRP3 protein levels in different disease models. Whether EPO-mediated neuroprotection after AIS is conveyed via an EPO/TAK1/inflammasome axis in microglia remains to be clarified. Subjecting mice deficient for TAK1 in microglia/macrophages (Mi/MΦ) to AIS revealed a significant reduction in infarct sizes and neurological impairments compared to the corresponding controls. Post-ischemic increased activation of TAK1, NLRP3, NLRC4, and AIM2 inflammasomes including their associated downstream cascades were markedly reduced upon deletion of Mi/MΦ TAK1. EPO administration improved clinical outcomes and dampened stroke-induced activation of TAK1 and inflammasome cascades, which was not evident after the deletion of Mi/MΦ TAK1. Pharmacological inhibition of NLRP3 in microglial BV-2 cells did not influence post-OGD IL-1β levels, but increased NLRC4 and AIM2 protein levels, suggesting compensatory activities among inflammasomes. Overall, we provide evidence that Mi/MΦ TAK1 regulates the expression and activation of the NLRP3, NLRC4, AIM2 inflammasomes. Furthermore, EPO mitigated stroke-induced activation of TAK1 and inflammasomes, indicating that EPO conveyed neuroprotection might be mediated via an EPO/TAK1/inflammasome axis.
000905217 536__ $$0G:(DE-HGF)POF4-5252$$a5252 - Brain Dysfunction and Plasticity (POF4-525)$$cPOF4-525$$fPOF IV$$x0
000905217 588__ $$aDataset connected to CrossRef, Journals: juser.fz-juelich.de
000905217 7001_ $$0P:(DE-HGF)0$$aZeyen, Thomas$$b1
000905217 7001_ $$0P:(DE-HGF)0$$aGoldmann, Tobias$$b2
000905217 7001_ $$0P:(DE-HGF)0$$aPrinz, Marco$$b3
000905217 7001_ $$0P:(DE-HGF)0$$aHuber, Michael$$b4
000905217 7001_ $$0P:(DE-HGF)0$$aJung, Jennifer$$b5
000905217 7001_ $$0P:(DE-HGF)0$$aArik, Eren$$b6
000905217 7001_ $$0P:(DE-HGF)0$$aHabib, Shahin$$b7
000905217 7001_ $$0P:(DE-HGF)0$$aSlowik, Alexander$$b8
000905217 7001_ $$0P:(DE-HGF)0$$aReich, Arno$$b9
000905217 7001_ $$0P:(DE-Juel1)171786$$aSchulz, Jörg B.$$b10
000905217 7001_ $$0P:(DE-HGF)0$$aHabib, Pardes$$b11$$eCorresponding author
000905217 773__ $$0PERI:(DE-600)2541897-X$$a10.1007/s12975-021-00948-8$$p 462–482$$tTranslational stroke research$$v13$$x1868-4483$$y2022
000905217 8564_ $$uhttps://juser.fz-juelich.de/record/905217/files/Heinisch2022_Article_ErythropoietinAbrogatesPost-Is.pdf$$yOpenAccess
000905217 909CO $$ooai:juser.fz-juelich.de:905217$$pdnbdelivery$$pdriver$$pVDB$$popen_access$$popenaire
000905217 9101_ $$0I:(DE-588b)5008462-8$$6P:(DE-Juel1)171786$$aForschungszentrum Jülich$$b10$$kFZJ
000905217 9131_ $$0G:(DE-HGF)POF4-525$$1G:(DE-HGF)POF4-520$$2G:(DE-HGF)POF4-500$$3G:(DE-HGF)POF4$$4G:(DE-HGF)POF$$9G:(DE-HGF)POF4-5252$$aDE-HGF$$bKey Technologies$$lNatural, Artificial and Cognitive Information Processing$$vDecoding Brain Organization and Dysfunction$$x0
000905217 9141_ $$y2022
000905217 915__ $$0LIC:(DE-HGF)CCBY4$$2HGFVOC$$aCreative Commons Attribution CC BY 4.0
000905217 915__ $$0StatID:(DE-HGF)0113$$2StatID$$aWoS$$bScience Citation Index Expanded$$d2021-02-03
000905217 915__ $$0StatID:(DE-HGF)3002$$2StatID$$aDEAL Springer$$d2021-02-03$$wger
000905217 915__ $$0StatID:(DE-HGF)0510$$2StatID$$aOpenAccess
000905217 915__ $$0StatID:(DE-HGF)0160$$2StatID$$aDBCoverage$$bEssential Science Indicators$$d2021-02-03
000905217 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR$$bTRANSL STROKE RES : 2021$$d2022-11-19
000905217 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS$$d2022-11-19
000905217 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline$$d2022-11-19
000905217 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bClarivate Analytics Master Journal List$$d2022-11-19
000905217 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection$$d2022-11-19
000905217 915__ $$0StatID:(DE-HGF)1110$$2StatID$$aDBCoverage$$bCurrent Contents - Clinical Medicine$$d2022-11-19
000905217 915__ $$0StatID:(DE-HGF)9905$$2StatID$$aIF >= 5$$bTRANSL STROKE RES : 2021$$d2022-11-19
000905217 9201_ $$0I:(DE-Juel1)INM-11-20170113$$kINM-11$$lJara-Institut Quantum Information$$x0
000905217 980__ $$ajournal
000905217 980__ $$aVDB
000905217 980__ $$aUNRESTRICTED
000905217 980__ $$aI:(DE-Juel1)INM-11-20170113
000905217 9801_ $$aFullTexts