Hexokinase cellular trafficking in ischemia-reperfusion and ischemic preconditioning is altered in type I diabetic heart

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dc.authorid0000-0002-1589-9229
dc.authorid0000-0001-7926-3089
dc.authorid0000-0002-0946-1407
dc.authorscopusid57115408300
dc.authorscopusid23975103000
dc.authorscopusid23974269300
dc.authorscopusid6505825773
dc.authorscopusid6602542683
dc.authorscopusid37102404100
dc.authorscopusid55662138900
dc.authorwosidGurevin, Ebru Gurel/AAC-7921-2020
dc.authorwosidDemirci-Tansel, Cihan/AAC-4534-2020
dc.authorwosidKapucu, Aysegul/AAC-7722-2020
dc.contributor.authorGürel, Ebru
dc.contributor.authorÜstünova, Savas
dc.contributor.authorKapucu, Ayşegül
dc.contributor.authorYılmazer, Nadim
dc.contributor.authorEerbeek, Otto
dc.contributor.authorNederlof, Rianne
dc.contributor.authorZuurbier, Coert J.
dc.date.accessioned2022-05-11T14:28:29Z
dc.date.available2022-05-11T14:28:29Z
dc.date.issued2013
dc.departmentFakülteler, Fen Edebiyat Fakültesi, Biyoloji Bölümü
dc.description.abstractDiabetes mellitus (DM) has been reported to alter the cardiac response to ischemia-reperfusion (IR). In addition, cardioprotection induced by ischemic preconditioning (IPC) is often impaired in diabetes. We have previously shown that the subcellular localisation of the glycolytic enzyme hexokinase (HK) is causally related to IR injury and IPC protective potential. Especially the binding of HK to mitochondria and prevention of HK solubilisation (HK detachment from mitochondria) during ischemia confers cardioprotection. It is unknown whether diabetes affects HK localisation during IR and IPC as compared to non-diabetes. In this study we hypothesize that DM alters cellular trafficking of hexokinase in response to IR and IPC, possibly explaining the altered response to IR and IPC in diabetic heart. Control (CON) and type I diabetic (DM) rat hearts (65 mg/kg streptozotocin, 4 weeks) were isolated and perfused in Langendorff-mode and subjected to 35 min I and 30 min R with or without IPC (3 times 5 min I). Cytosolic and mitochondrial fractions were obtained at (1) baseline, i.e. after IPC but before I, (2) 35 min I, (3) 5 min R and (4) 30 min R. DM improved rate-pressure product recovery (RPP; 71 +/- A 10 % baseline (DM) versus 9 +/- A 1 % baseline (CON) and decreased contracture (end-diastolic pressure: 24 +/- A 8 mmHg (DM) vs 77 +/- A 4 mmHg (CON)) after IR as compared to control, and was associated with prevention of HK solubilisation at 35 min I. IPC improved cardiac function in CON but not in DM hearts. IPC in CON prevented HK solubilisation at 35 min I and at 5 min R, with a trend for increased mitochondrial HK. In contrast, the non-effective IPC in DM was associated with solubilisation of HK and decreased mitochondrial HK at early reperfusion and a reciprocal behaviour at late reperfusion. We conclude that type I DM significantly altered cellular HK translocation patterns in the heart in response to IR and IPC, possibly explaining altered response to IR and IPC in diabetes.
dc.description.sponsorshipScientific and Technological Research Council of Turkey (TUBITAK)Turkiye Bilimsel ve Teknolojik Arastirma Kurumu (TUBITAK) [TBAG-107T212]; Scientific Research Projects Coordination Unit of Istanbul UniversityIstanbul University [UDP-16146, UDP-25255]
dc.description.sponsorshipThis study was supported by The Scientific and Technological Research Council of Turkey (TUBITAK) (Project No: TBAG-107T212) and by Scientific Research Projects Coordination Unit of Istanbul University (Grants UDP-16146, UDP-25255).
dc.identifier.doi10.1007/s11033-013-2495-5
dc.identifier.endpage4160
dc.identifier.issn0301-4851
dc.identifier.issn1573-4978
dc.identifier.issue7en_US
dc.identifier.pmid23652994
dc.identifier.scopus2-s2.0-84879390835
dc.identifier.scopusqualityQ2
dc.identifier.startpage4153
dc.identifier.urihttps://doi.org/10.1007/s11033-013-2495-5
dc.identifier.urihttps://hdl.handle.net/20.500.11776/6846
dc.identifier.volume40
dc.identifier.wosWOS:000320674700003
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.institutionauthorYılmazer, Nadim
dc.language.isoen
dc.publisherSpringer
dc.relation.ispartofMolecular Biology Reports
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectDiabetes
dc.subjectIschemia-reperfusion
dc.subjectCardioprotection
dc.subjectMitochondrial Hexokinase
dc.subjectInduced Cardioprotection
dc.subjectInsulin
dc.subjectProtection
dc.subjectInjury
dc.subjectOverexpression
dc.subjectCardiomyocytes
dc.subjectMetabolism
dc.subjectMechanism
dc.subjectGlucose
dc.titleHexokinase cellular trafficking in ischemia-reperfusion and ischemic preconditioning is altered in type I diabetic heart
dc.typeArticle

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