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dc.contributor.author Hosszú, Ádám
dc.contributor.author Antal, Zsuzsanna
dc.contributor.author Lénárt, Lilla
dc.contributor.author Hodrea, Judit
dc.contributor.author Kőszegi, Sándor
dc.contributor.author Balogh, Dóra Bianka
dc.contributor.author Bánki, Nóra Fanni
dc.contributor.author Wágner, László József
dc.contributor.author Dénes, Ádám
dc.contributor.author Hamar, Péter
dc.contributor.author Degrell P
dc.contributor.author Vannay, Ádám
dc.contributor.author Szabó, Attila
dc.contributor.author Fekete, Andrea
dc.date.accessioned 2017-03-27T12:39:53Z
dc.date.available 2017-03-27T12:39:53Z
dc.date.issued 2017
dc.identifier.citation pagination=152-165; journalVolume=28; journalIssueNumber=1; journalTitle=JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY;
dc.identifier.uri http://repo.lib.semmelweis.hu//handle/123456789/4073
dc.identifier.uri doi:10.1681/ASN.2015070772
dc.description.abstract Mechanisms of renal ischemia-reperfusion injury remain unresolved, and effective therapies are lacking. We previously showed that dehydroepiandrosterone protects against renal ischemia-reperfusion injury in male rats. Here, we investigated the potential role ofsigma1-receptor activation in mediating this protection. In rats, pretreatment with either dehydroepiandrosterone or fluvoxamine, a high-affinitysigma1-receptor agonist, improved survival, renal function and structure, and the inflammatory response after sublethal renal ischemia-reperfusion injury. In human proximal tubular epithelial cells, stimulation by fluvoxamine or oxidative stress caused thesigma1-receptor to translocate from the endoplasmic reticulum to the cytosol and nucleus. Fluvoxamine stimulation in these cells also activated nitric oxide production that was blocked bysigma1-receptor knockdown or Akt inhibition. Similarly, in the postischemic rat kidney,sigma1-receptor activation by fluvoxamine triggered the Akt-nitric oxide synthase signaling pathway, resulting in time- and isoform-specific endothelial and neuronal nitric oxide synthase activation and nitric oxide production. Concurrently, intravital two-photon imaging revealed prompt peritubular vasodilation after fluvoxamine treatment, which was blocked by thesigma1-receptor antagonist or various nitric oxide synthase blockers. In conclusion, in this rat model of ischemia-reperfusion injury,sigma1-receptor agonists improved postischemic survival and renal functionviaactivation of Akt-mediated nitric oxide signaling in the kidney. Thus,sigma1-receptor activation might provide a therapeutic option for renoprotective therapy.
dc.relation.ispartof urn:issn:1046-6673
dc.title Sigma1-Receptor Agonism Protects against Renal Ischemia-Reperfusion Injury
dc.type Journal Article
dc.date.updated 2017-02-03T12:02:12Z
dc.language.rfc3066 en
dc.identifier.mtmt 3049309
dc.identifier.pubmed 27056295
dc.contributor.department SE/AOK/K/I. Sz. Gyermekgyógyászati Klinika
dc.contributor.department SE/AOK/K/ISZGYK/MTA-SE Gyermekgyógyászati és Nephrológiai Kutatócsoport
dc.contributor.department SE/AOK/K/ISZGYK/MTA-SE Lendület Diabétesz Kutatócsoport
dc.contributor.department SE/AOK/I/Kórélettani Intézet
dc.contributor.department SE/AOK/K/Transzplantációs és Sebészeti Klinika
dc.contributor.institution Semmelweis Egyetem


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