8-Br-cADPR,a TRPM2 ion channel antagonist, inhibits renal ischemia-reperfusion injury

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dc.authorid0000-0003-2424-2269
dc.authorscopusid57190794932
dc.authorscopusid57191852988
dc.authorscopusid56727936300
dc.authorscopusid56727936300
dc.authorwosidEraslan, Ersen/ABC-5840-2020
dc.contributor.authorEraslan, Ersen
dc.contributor.authorTanyeli, Ayhan
dc.contributor.authorPolat, Elif
dc.contributor.authorPolat, Elif
dc.date.accessioned2022-05-11T14:42:04Z
dc.date.available2022-05-11T14:42:04Z
dc.date.issued2019
dc.departmentFakülteler, Tıp Fakültesi, Temel Tıp Bilimleri Bölümü, Histoloji ve Embriyoloji Ana Bilim Dalı
dc.description.abstractThe transient receptor potential melastatin-2 (TRPM2) channel belongs to the transient receptor potential channel superfamily and is a cation channel permeable to Na+ and Ca (2+). The TRPM2 ion channel is expressed in the kidney and can be activated by various molecules such as hydrogen peroxide, calcium, and cyclic adenosine diphosphate (ADP)-ribose (cADPR) that are produced during acute kidney injury. In this study, we investigated the role of 8-bromo-cyclic ADP-ribose (8-Br-cADPR; a cADPR antagonist) in renal ischemia-reperfusion injury using biochemical and histopathological parameters. CD38, cADPR, tumor necrosis factor-, interleukin-1, and myeloperoxidase (inflammatory markers), urea and creatinine, hydrogen peroxide (oxidant), and catalase (antioxidant enzyme) levels that increase with ischemia-reperfusion injury decreased in the groups treated with 8-Br-cADPR. In addition, renin levels were elevated in the groups treated with 8-Br-cADPR. Histopathological examination revealed that 8-Br-cADPR reduced renal damage and the expression of caspase-3 and TRPM2. Our results suggest that the inhibition of TRPM2 ion channel may be a new treatment modality for ischemic acute kidney injury.
dc.description.sponsorshipAtaturk UniversitesiAtaturk University [2014-146]
dc.description.sponsorshipAtaturk Universitesi, Grant/Award Number: 2014-146
dc.identifier.doi10.1002/jcp.27236
dc.identifier.endpage4581
dc.identifier.issn0021-9541
dc.identifier.issn1097-4652
dc.identifier.issue4en_US
dc.identifier.pmid30191993
dc.identifier.scopus2-s2.0-85052960369
dc.identifier.scopusqualityQ1
dc.identifier.startpage4572
dc.identifier.urihttps://doi.org/10.1002/jcp.27236
dc.identifier.urihttps://hdl.handle.net/20.500.11776/9200
dc.identifier.volume234
dc.identifier.wosWOS:000457613700118
dc.identifier.wosqualityQ1
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.institutionauthorPolat, Elif
dc.language.isoen
dc.publisherWiley
dc.relation.ispartofJournal of Cellular Physiology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subject8-Br-cADPR
dc.subjectcytokines
dc.subjectischemia-reperfusion
dc.subjectoxidative stress
dc.subjectTRPM2
dc.subjectCyclic-Adp-Ribose
dc.subjectIntracellular Free Calcium
dc.subjectCaspase-3 Gene-Expression
dc.subjectOxidative Stress
dc.subjectIschemia/Reperfusion Injury
dc.subjectRyanodine Receptor
dc.subjectMolecular-Cloning
dc.subjectOxidant Stress
dc.subjectKidney Injury
dc.subjectMice Lacking
dc.title8-Br-cADPR,a TRPM2 ion channel antagonist, inhibits renal ischemia-reperfusion injury
dc.typeArticle

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