Document Detail

Myocardial release of FKBP12 and increased production of FKBP12.6 in ischemia and reperfusion experimental models.
MedLine Citation:
PMID:  19878648     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: Coronary artery occlusion and reperfusion may trigger reversible and irreversible ischemic and reperfusion injury. The primary aim of this study was to evaluate protein release into the myocardium in a porcine model during ischemia and reperfusion to search for clarifying models for reperfusion injury and secondarily to investigate release and production of the immunophilins FKBP12/12.6 in this model and in cell cultures. METHODS: In a porcine model local myocardial ischemia was induced during 45min followed by 120min of reperfusion. Microdialysis samples from ischemic and non-ischemic areas were analyzed with surface-enhanced laser desorption ionization (SELDI) mass spectrometry (MS) and Western blotting (WB). Myocardial biopsies from areas at risk and control areas were analyzed with reverse transcription polymerase chain reaction (RT-PCR). Myocardial cell cultures from mice (HL-1 cells) were exposed to hypoxia and then analyzed with WB and RT-PCR. RESULTS: FK binding protein12 (FKBP12), ubiquitin and myoglobin were identified as being released during ischemia and reperfusion in microdialysates. RT-PCR analysis on the biopsies after ischemia revealed a non-significant increase in mRNA expression of FKBP12 and a significant increase in mRNA expression of FKBP12.6. Lysates from HL-1 cells exposed to hypoxia demonstrated increase of FKBP12 and a significant increase in mRNA expression of FKBP12.6. CONCLUSION: In a myocardial ischemic-reperfusion porcine model as well as in hypoxic HL-1 cells, release of FKBP12 and increased production of FKBP12.6 was demonstrated. The findings indicate important mechanisms related to these immunophilins in the reaction to ischemia/hypoxia and reperfusion in the heart.
Karin Aström-Olsson; Lars Karlsson; Lillemor Mattsson Hultén; Pia Davidsson; Vittorio Mantovani; Chrichan Månsson; Sven-Olof Olofsson; Olov Wiklund; Lars Grip
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-10-28
Journal Detail:
Title:  Biochemical and biophysical research communications     Volume:  390     ISSN:  1090-2104     ISO Abbreviation:  Biochem. Biophys. Res. Commun.     Publication Date:  2009 Dec 
Date Detail:
Created Date:  2009-11-30     Completed Date:  2010-01-12     Revised Date:  2010-01-21    
Medline Journal Info:
Nlm Unique ID:  0372516     Medline TA:  Biochem Biophys Res Commun     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1299-304     Citation Subset:  IM    
Department of Cardiology, Sahlgrenska University Hospital, Gothenburg, Sweden.
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MeSH Terms
Cell Line
Disease Models, Animal
Myocardial Reperfusion Injury / metabolism*
Myocardium / metabolism
Tacrolimus Binding Protein 1A / metabolism*
Tacrolimus Binding Proteins / biosynthesis*
Reg. No./Substance:
EC 5.2.1.-/Tacrolimus Binding Protein 1A; EC 5.2.1.-/Tacrolimus Binding Proteins; EC 5.2.1.-/tacrolimus binding protein 1B

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