The effect of chronic doxorubicin treatment on mitogen-activated protein kinases and heat stress proteins in rat hearts
Jazyk angličtina Země Česko Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
18373386
DOI
10.33549/physiolres.931558
PII: 1558
Knihovny.cz E-zdroje
- MeSH
- chaperon hsp60 metabolismus MeSH
- doxorubicin MeSH
- extracelulárním signálem regulované MAP kinasy metabolismus MeSH
- fosforylace MeSH
- kontrakce myokardu MeSH
- krysa rodu Rattus MeSH
- mitogenem aktivované proteinkinasy p38 metabolismus MeSH
- modely nemocí na zvířatech MeSH
- myokard enzymologie MeSH
- nádorové proteiny metabolismus MeSH
- nemoci srdce chemicky indukované enzymologie patofyziologie MeSH
- proteiny tepelného šoku HSP27 MeSH
- proteiny tepelného šoku HSP70 metabolismus MeSH
- proteiny tepelného šoku HSP90 metabolismus MeSH
- proteiny teplotního šoku metabolismus MeSH
- protinádorová antibiotika MeSH
- reperfuzní poškození myokardu enzymologie patofyziologie 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
- chaperon hsp60 MeSH
- doxorubicin MeSH
- extracelulárním signálem regulované MAP kinasy MeSH
- Hspb1 protein, rat MeSH Prohlížeč
- mitogenem aktivované proteinkinasy p38 MeSH
- nádorové proteiny MeSH
- proteiny tepelného šoku HSP27 MeSH
- proteiny tepelného šoku HSP70 MeSH
- proteiny tepelného šoku HSP90 MeSH
- proteiny teplotního šoku MeSH
- protinádorová antibiotika MeSH
The study has been designed to characterize protein systems involved in the responses of rat hearts to chronic doxorubicin (DOX) treatment. We investigated the influence of DOX on cardiac function, mitogen-activated protein kinases (MAPKs) and heat stress proteins (HSPs). Doxorubicin was administered to rats by intraperitoneal injections over a period of 6 weeks. In control and DOX-treated hearts exposed to 20 min global ischemia and 40 min reperfusion the recovery of contractile function after ischemia/reperfusion (I/R) was determined. The levels and phosphorylation state of proteins in tissue samples were analyzed using specific antibodies. We found an activation of extracellular signal-regulated kinases (ERKs) in rat hearts exposed to DOX treatment and better recovery of contractile function after I/R. Analysis of HSPs showed that DOX induced up-regulation of the levels of HSP60 and down-regulation of HSP70 levels. The levels and/or specific phosphorylation of other studied proteins (p38-MAPK, HSP27, HSP90) were not influenced by DOX. The results point to the possible role of ERKs and some HSPs in mechanisms underlying the response of rat hearts to chronic DOX treatment.
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