Selenium prevents interferon-gamma induced activation of TRPM2 channel and inhibits inflammation, mitochondrial oxidative stress, and apoptosis in microglia

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dc.authoridakyuva, yener/0000-0001-8171-5929
dc.authoridYILDIZHAN, Kenan/0000-0002-6585-4010
dc.authoridNAZIROGLU, Mustafa/0000-0003-0887-6974
dc.contributor.authorAkyuva, Yener
dc.contributor.authorNaziroglu, Mustafa
dc.contributor.authorYildizhan, Kenan
dc.date.accessioned2024-09-18T20:02:34Z
dc.date.available2024-09-18T20:02:34Z
dc.date.issued2021
dc.departmentHatay Mustafa Kemal Üniversitesien_US
dc.description.abstractMicroglia as the primary immune cells of brain act protective effects against injuries and infections in the central nervous system. Inflammation via excessive Ca(2+)influx and oxygen radical species (ROS) generation is a known factor in many neurodegenerative disorders. Importantly, the Ca(2+)permeable TRPM2 channel is activated by oxidative stress. Thus, TRPM2 could provide the excessive Ca(2+)influx in the microglia. Although TRPM2 expression level is high in inflammatory cells, the interplay between mouse microglia and TRPM2 channel during inflammation is not fully identified. Thus, it is important to understand the mechanisms and factors involved in order to enhance neuronal regeneration and repair. The data presented here indicate that TRPM2 channels were activated in microglia cells by interferon-gamma (IFN gamma). The IFN gamma treatment further increased apoptosis (early and late) and cytokine productions (TNF-alpha, IL-1 beta, and IL-6) which were due to increased lipid peroxidation and ROS generations as well as increased activations of caspase -3 (Casp-3) and - 9 (Casp-9). However, selenium treatment diminished activations of TRPM2, cytokine, Casp-3, and Casp-9, and levels of lipid peroxidation and mitochondrial ROS production in the microglia that were treated with IFN gamma. Moreover, addition of either PARP1 inhibitors (PJ34 or DPQ) or TRPM2 blockers (2-APB or ACA) potentiated the modulator effects of selenium. These results clearly suggest that IFN gamma leads to TRPM2 activation in microglia cells; whereas, selenium prevents IFN gamma-mediated TRPM2 activation and cytokine generation. Together the interplay between IFN gamma released from microglia cells is importance in brain inflammation and may affect oxidative cytotoxicity in the microglia.en_US
dc.description.sponsorshipBSN Health, Analyses, Innovation, Consultancy, Organization, Agriculture and Industry Ltd., Goller Bolgesi Teknokenti, Isparta, Turkey [2018-30]en_US
dc.description.sponsorshipThe study was supported by BSN Health, Analyses, Innovation, Consultancy, Organization, Agriculture and Industry Ltd., Goller Bolgesi Teknokenti, Isparta, Turkey (Project No: 2018-30). There is no financial disclosure of the current study.en_US
dc.identifier.doi10.1007/s11011-020-00624-0
dc.identifier.endpage298en_US
dc.identifier.issn0885-7490
dc.identifier.issn1573-7365
dc.identifier.issue2en_US
dc.identifier.pmid33044639en_US
dc.identifier.scopus2-s2.0-85092483541en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage285en_US
dc.identifier.urihttps://doi.org/10.1007/s11011-020-00624-0
dc.identifier.urihttps://hdl.handle.net/20.500.12483/7874
dc.identifier.volume36en_US
dc.identifier.wosWOS:000577058700001en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherSpringer/Plenum Publishersen_US
dc.relation.ispartofMetabolic Brain Diseaseen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectApoptosisen_US
dc.subjectInflammationen_US
dc.subjectMicrogliaen_US
dc.subjectMitochondriaen_US
dc.subjectTRPM2 channelen_US
dc.titleSelenium prevents interferon-gamma induced activation of TRPM2 channel and inhibits inflammation, mitochondrial oxidative stress, and apoptosis in microgliaen_US
dc.typeArticleen_US

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