Cardiac protection by mitoK(ATP) channels is dependent on akt translocation from cytosol to mitochondria during late preconditioning

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dc.authorid0000-0003-1380-350X
dc.contributor.authorAhmad, Nauman
dc.contributor.authorWang, Yigang
dc.contributor.authorHaider, Khawaja Husnain
dc.contributor.authorWang, Boyu
dc.contributor.authorPasha, Zeeshan
dc.contributor.authorUzun, Özge
dc.contributor.authorAshraf, Muhammad
dc.date.accessioned2021-06-23T19:19:05Z
dc.date.available2021-06-23T19:19:05Z
dc.date.issued2006
dc.departmentBAİBÜ, Tıp Fakültesi, Dahili Tıp Bilimleri Bölümüen_US
dc.description.abstractThis investigation elucidates the Akt/mitochondrial ATP-sensitive K+ (mitoK(ATP)) channel signaling pathway in late pharmacological preconditioning, using the mitoK(ATP) channel openers BMS-191095 (BMS) and diazoxide (DE). BMS (1 mg/kg ip) and DE (7 mg/kg ip) alone or BMS plus wortmannin (WTN, 15 mu g/kg ip), an inhibitor of phosphatidylinositol 3-kinase, and BMS plus 5-hydroxydecanoic acid (5-HD, 5 mg/kg ip), an inhibitor of mitoK(ATP) channels, were administered to male mice. Twenty-four hours later, hearts were isolated and subjected to 40 min of ischemia and 120 min of reperfusion via Langendorff's apparatus. Both BMS and DE reduced left ventricular end-diastolic pressure and increased left ventricular developed pressure as well as reduced LDH release. Coadministration of BMS and WTN abolished the beneficial effects of BMS on cardiac function. Moreover, BMS and DE accelerated Akt phosphorylation in cardiac tissue as determined by Western blot analysis and also significantly reduced apoptosis compared with ischemic control. WTN significantly suppressed BMS-induced Akt phosphorylation, whereas 5-HD had no effect on Akt phosphorylation in cytosol, and the effect of BMS on apoptosis was abolished. It is concluded that the cardioprotective effect by mitoK(ATP) channels is attributed to the translocation of phosphorylated Akt from cytosol to mitochondria.en_US
dc.identifier.doi10.1152/ajpheart.00737.2005
dc.identifier.endpageH2408en_US
dc.identifier.issn0363-6135
dc.identifier.issn1522-1539
dc.identifier.issue6en_US
dc.identifier.pmid16687609en_US
dc.identifier.scopus2-s2.0-33744918504en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.startpageH2402en_US
dc.identifier.urihttps://doi.org/10.1152/ajpheart.00737.2005
dc.identifier.urihttps://hdl.handle.net/20.500.12491/5870
dc.identifier.volume290en_US
dc.identifier.wosWOS:000237419600032en_US
dc.identifier.wosqualityQ1en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.institutionauthorUzun, Özge
dc.language.isoenen_US
dc.publisherAmer Physiological Socen_US
dc.relation.ispartofAmerican Journal Of Physiology-Heart And Circulatory Physiologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectBMS-191095en_US
dc.subjectDiazoxideen_US
dc.subjectApoptosisen_US
dc.subjectMitochondrial ATP-sensitive K Channelsen_US
dc.titleCardiac protection by mitoK(ATP) channels is dependent on akt translocation from cytosol to mitochondria during late preconditioningen_US
dc.typeArticleen_US

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