Cardioprotective adaptation of rats to intermittent hypobaric hypoxia is accompanied by the increased association of hexokinase with mitochondria
Jazyk angličtina Země Spojené státy americké Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
26494452
DOI
10.1152/japplphysiol.01035.2014
PII: japplphysiol.01035.2014
Knihovny.cz E-zdroje
- Klíčová slova
- cardioprotection, chronic hypoxia, hexokinase, mitochondria colocalization, rat heart,
- MeSH
- fyziologická adaptace * MeSH
- hematokrit MeSH
- hexokinasa metabolismus MeSH
- hypoxie enzymologie patofyziologie MeSH
- izoenzymy metabolismus MeSH
- krysa rodu Rattus MeSH
- mitochondrie enzymologie MeSH
- myokard enzymologie MeSH
- potkani Wistar MeSH
- tělesná hmotnost MeSH
- tlak vzduchu MeSH
- velikost orgánu MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- hexokinasa MeSH
- izoenzymy MeSH
Chronic hypoxia increases the myocardial resistance to acute ischemia-reperfusion injury by affecting the mitochondrial redox balance. Hexokinase (HK) bears a high potential to suppress the excessive formation of reactive oxygen species because of its increased association with mitochondria, thereby inhibiting the membrane permeability transition pore opening and preventing cell death. The purpose of this study was to determine the effect of severe intermittent hypobaric hypoxia (7,000 m, 8 h/day, 5 wk) on the function and colocalization of HK isoforms with mitochondria in the left (LV) and right ventricles of rat myocardium. The real-time RT-PCR, Western blot, enzyme coupled assay, and quantitative immunofluorescence techniques were used. Our results showed significantly elevated expression of HK isoforms (HK1 and HK2) in the hypoxic LV. In addition, intermittent hypoxia increased the total HK activity and the association of HK isoforms with mitochondria in both ventricles. These findings suggest that HK may contribute to the cardioprotective phenotype induced by adaptation to severe intermittent hypobaric hypoxia.
Department of Physiology Faculty of Science Charles University Prague Prague Czech Republic; and
Institute of Physiology Czech Academy of Sciences Prague Czech Republic
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