Chronic hypoxia enhances expression and activity of mitochondrial creatine kinase and hexokinase in the rat ventricular myocardium
Jazyk angličtina Země Německo Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
24525799
DOI
10.1159/000356671
PII: 000356671
Knihovny.cz E-zdroje
- MeSH
- chronická nemoc MeSH
- energetický metabolismus MeSH
- hexokinasa biosyntéza MeSH
- hypoxie enzymologie patologie MeSH
- kreatinkinasa biosyntéza MeSH
- krysa rodu Rattus MeSH
- mitochondriální proteiny biosyntéza MeSH
- myokard enzymologie patologie MeSH
- potkani Wistar MeSH
- regulace genové exprese enzymů * MeSH
- srdeční komory enzymologie patologie MeSH
- srdeční mitochondrie enzymologie patologie 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
- kreatinkinasa MeSH
- mitochondriální proteiny MeSH
BACKGROUND: Creatine kinase (CK) and hexokinase (HK) play a key role in myocardial energy homeostasis. We aimed to determine CK and HK expression and enzyme activity in the left (LV) and right (RV) ventricles of rats adapted for 3 weeks to normobaric hypoxia (10 % O2) either continuously (CNH) or intermittently with 1-h or 16-h normoxic episode per day. METHODS: The Real-Time RT-PCR, Western blot, and enzyme-coupled assays were used. In addition, the effect of CNH on the HK co-localization with mitochondria, which can inhibit apoptosis, was assessed using immunofluorescence techniques. RESULTS: CK and HK activities increased in the LV during all hypoxic adaptations, which was consistent with elevated protein levels of mitochondrial mtCKs, cytosolic CKB, HK1, and HK2 isoforms. Enzyme activities also increased in the hypoxic RV, but only CKB protein was elevated. No effect of CNH on HK1 or HK2 co-localization with mitochondria was observed. CONCLUSION: Up-regulation of mtCKs and HK isoforms may stimulate the respiratory chain and help to maintain energy homeostasis of chronically hypoxic myocardium and prevent oxidative stress. In this way, CK and HK enzymes can possibly participate in the establishment of ischemia-resistant phenotype of chronically hypoxic hearts.
Citace poskytuje Crossref.org
Sixty Years of Heart Research in the Institute of Physiology of the Czech Academy of Sciences
Desmin Knock-Out Cardiomyopathy: A Heart on the Verge of Metabolic Crisis