PMID- 19228992
OWN - NLM
STAT- MEDLINE
DCOM- 20090707
LR  - 20130926
IS  - 8750-7587 (Print)
IS  - 0161-7567 (Linking)
VI  - 106
IP  - 6
DP  - 2009 Jun
TI  - Ischemic preconditioning affects hexokinase activity and HKII in different 
      subcellular compartments throughout cardiac ischemia-reperfusion.
PG  - 1909-16
LID - 10.1152/japplphysiol.90537.2008 [doi]
AB  - The glycolytic enzyme hexokinase (HK) is suggested to play a role in ischemic 
      preconditioning (IPC). In the present study we determined how ischemic 
      preconditioning affects HK activity and HKI and HKII protein content at five 
      different time points and three different subcellular fractions throughout 
      cardiac ischemia-reperfusion. Isolated Langendorff-perfused rat hearts (10 groups 
      of 7 hearts each) were subjected to 35 min ischemia and 30 min reperfusion 
      (control groups); the IPC groups were pretreated with 3 times 5-min ischemia. IPC 
      was without effect on microsomal HK activity, and only decreased cytosolic HK 
      activity at 35 min ischemia, which was mimicked by decreased cytosolic HKII, but 
      not HKI, protein content. In contrast, mitochondrial HK activity at baseline and 
      during reperfusion was elevated by IPC, without changes during ischemia. No 
      effect of IPC on mitochondrial HK I protein content was observed. However, 
      mitochondrial HK II protein content during reperfusion was augmented by IPC, 
      albeit not following the IPC stimulus. It is concluded that IPC results in 
      decreased cytosolic HK activity during ischemia that could be explained by 
      decreased HKII protein content. IPC increased mitochondrial HK activity before 
      ischemia and during reperfusion that was only mimicked by increased HK II protein 
      content during reperfusion. IPC was without effect on the phosphorylation status 
      of HK before ischemia. We conclude that IPC is associated with 1) a biphasic 
      response of increased mitochondrial HK activity before and after ischemia, 2) 
      decreased cytosolic HK activity during ischemia, and 3) cellular redistribution 
      of HKII but not HKI.
FAU - Gurel, Ebru
AU  - Gurel E
AD  - Department of Anaesthesiology, University of Amsterdam, Meibergdreef 9, 1105 AZ 
      Amsterdam, The Netherlands.
FAU - Smeele, Kirsten M
AU  - Smeele KM
FAU - Eerbeek, Otto
AU  - Eerbeek O
FAU - Koeman, Anneke
AU  - Koeman A
FAU - Demirci, Cihan
AU  - Demirci C
FAU - Hollmann, Markus W
AU  - Hollmann MW
FAU - Zuurbier, Coert J
AU  - Zuurbier CJ
LA  - eng
PT  - Journal Article
DEP - 20090219
PL  - United States
TA  - J Appl Physiol (1985)
JT  - Journal of applied physiology (Bethesda, Md. : 1985)
JID - 8502536
RN  - EC 2.7.1.1 (Hexokinase)
SB  - IM
MH  - Animals
MH  - Cell Fractionation
MH  - Cellular Structures/*enzymology
MH  - Cytosol/enzymology
MH  - Hexokinase/*metabolism
MH  - *Ischemic Preconditioning, Myocardial
MH  - Male
MH  - Mitochondria, Heart/enzymology
MH  - Myocardial Reperfusion Injury/*enzymology/physiopathology
MH  - Rats
MH  - Rats, Wistar
EDAT- 2009/02/21 09:00
MHDA- 2009/07/08 09:00
CRDT- 2009/02/21 09:00
PHST- 2009/02/21 09:00 [entrez]
PHST- 2009/02/21 09:00 [pubmed]
PHST- 2009/07/08 09:00 [medline]
AID - 90537.2008 [pii]
AID - 10.1152/japplphysiol.90537.2008 [doi]
PST - ppublish
SO  - J Appl Physiol (1985). 2009 Jun;106(6):1909-16. doi: 
      10.1152/japplphysiol.90537.2008. Epub 2009 Feb 19.