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Evidence that activation of P2X7R does not exacerbate neuronal death after optic nerve transection and focal cerebral ischemia in mice

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dc.contributor.authorCaglayan, Berrak
dc.contributor.authorCaglayan, Ahmet B.
dc.contributor.authorBeker, Mustafa C.
dc.contributor.authorYalcin, Esra
dc.contributor.authorBEKER, MERVE
dc.contributor.authorKelestemur, Taha
dc.contributor.authorSertel, Elif
dc.contributor.authorÖZTÜRK, GÜRKAN
dc.contributor.authorKilic, Ulkan
dc.contributor.authorŞAHİN, FİKRETTİN
dc.contributor.authorKILIÇ, ERTUĞRUL
dc.contributor.institutionauthorBEKER, MERVE
dc.date.accessioned2020-10-22T15:55:46Z
dc.date.available2020-10-22T15:55:46Z
dc.date.issued2017-10-01T00:00:00Z
dc.description.abstractConflicting data in the literature about the function of P2X7R in survival following ischemia necessitates the conductance of in-depth studies. To investigate the impacts of activation vs inhibition of the receptor on neuronal survival as well as the downstream signaling cascades, in addition to optic nerve transection (ONT), 30 min and 90 min of middle cerebral artery occlusion (MCAo) models were performed in mice. Intracellular calcium levels were assessed in primary cortical neuron cultures. Here, we show that P2X7R antagonist Brilliant Blue G (BBG) decreased DNA fragmentation, infarct volume, brain swelling, neurological deficit scores and activation of microglial cells after focal cerebral ischemia. BBG also significantly increased the number of surviving retinal ganglion cells (RGCs) after ONT and the number of surviving neurons following MCAo. Importantly, receptor agonist BzATP resulted in increased activation of microglial cells and induced phosphorylation of ERK,AKT and JNK. These results indicated that inhibition of P2X7R with BBG promoted neuronal survival, not through the activation of survival kinase pathways, but possibly by improved intracellular Ca2+ overload and decreased the levels of Caspase 1, IL-1 beta and Bax proteins. On the other hand, BzATP-mediated increased number of activated microglia and increased survival kinase levels in addition to increased caspase-1 and IL-1 beta levels indicate the complex nature of the P2X7 receptor-mediated signaling in neuronal injury. (C) 2017 Elsevier Inc. All rights reserved.
dc.identifier.citationCaglayan B., Caglayan A. B. , Beker M. C. , Yalcin E., BEKER M., Kelestemur T., Sertel E., ÖZTÜRK G., Kilic U., ŞAHİN F., et al., -Evidence that activation of P2X7R does not exacerbate neuronal death after optic nerve transection and focal cerebral ischemia in mice-, EXPERIMENTAL NEUROLOGY, cilt.296, ss.23-31, 2017
dc.identifier.doi10.1016/j.expneurol.2017.06.024
dc.identifier.pubmed28669743
dc.identifier.scopus85021686881
dc.identifier.urihttp://hdl.handle.net/20.500.12645/23668
dc.identifier.wosWOS:000408296600003
dc.titleEvidence that activation of P2X7R does not exacerbate neuronal death after optic nerve transection and focal cerebral ischemia in mice
dc.typeArticle
dspace.entity.typePublication
local.avesis.id4cf35ef6-73ce-4adb-9851-249f1c1b1bf1
local.publication.goal16 - Barış, Adalet ve Güçlü Kurumlar
local.publication.isinternational1
relation.isAuthorOfPublication6f8a3a29-68af-47b4-b206-bbc6051b00f5
relation.isAuthorOfPublication.latestForDiscovery6f8a3a29-68af-47b4-b206-bbc6051b00f5
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relation.isGoalOfPublication.latestForDiscovery7e7ce1dc-9556-4fa2-b604-c2ba181d38b9
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