NDLI: Hexokinase cellular trafficking in ischemia–reperfusion and ischemic preconditioning is altered in type I diabetic heart

Content Provider	Springer Nature Link
Author	Gurel, Ebru Ustuva, Savas Kapucu, Aysegul Yilmazer, Nadim Eerbeek, Otto Nederlof, Rianne Hollmann, Markus W. Demirci Tansel, Cihan Zuurbier, Coert J.
Copyright Year	2013
Abstract	Diabetes 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 ± 10 % baseline (DM) versus 9 ± 1 % baseline (CON) and decreased contracture (end-diastolic pressure: 24 ± 8 mmHg (DM) vs 77 ± 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.
Starting Page	4153
Ending Page	4160
Page Count	8
File Format	PDF
ISSN	03014851
Journal	Molecular Biology Reports
Volume Number	40
Issue Number	7
e-ISSN	15734978
Language	English
Publisher	Springer Netherlands
Publisher Date	2013-05-08
Publisher Place	Dordrecht
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Diabetes Ischemia–reperfusion Cardioprotection Animal Anatomy / Morphology / Histology Animal Biochemistry
Content Type	Text
Resource Type	Article
Subject	Genetics Medicine Molecular Biology

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