Document Detail


Reduction of hypoxia-inducible heme oxygenase-1 in the myocardium after left ventricular mechanical support.
MedLine Citation:
PMID:  12015748     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Left ventricular assist devices (LVAD) may improve cardiac function. The pathogenesis of this phenomenon, called 'reverse remodelling', is not completely elucidated. To examine the hypothesis that LVAD support eliminates tissue stress by reducing local hypoxia, the distribution of heme oxygenase-1 (HO-1), a stress protein inducible by hypoxia, was examined in vivo and in vitro. The immunoreactivity for HO-1 was semi-quantitatively analysed in left ventricular tissue of 23 patients (14 dilated cardiomyopathy (DCM), six ischaemic heart disease (IHD), three myocarditis/congenital heart disease) with end-stage heart failure before and after LVAD support, while two unused donor hearts served as controls. Control hearts stained almost negative for HO-1, while failing hearts showed immunoreactivity mainly in cardiomyocytes, but also in endothelial cells, some smooth muscle cells and fibroblasts. Hearts with IHD showed significantly higher HO-1 immunoreactivity than hearts with DCM or myocarditis/congenital heart disease. After LVAD support, the HO-1 content decreased significantly in the DCM and IHD group and was significantly higher in the subendocardium than in the subepicardium. In vitro, under hypoxic conditions, neonatal rat cardiomyocytes showed an increase of HO-1 protein content up to sixfold above the normal level, which returned to normal values after normoxic cultivation. Mechanical support reduces the HO-1 content of the failing heart and HO-1 is inducible in vitro under hypoxia and is reversible under normoxia. This supports the concept that restoration of cardiac normoxia by mechanical unloading, particularly in the subendocardium, may be in part responsible for the phenomenon of 'reverse remodelling'.
Authors:
Florian Grabellus; Christof Schmid; Bodo Levkau; Dirk Breukelmann; Philip F Halloran; Christian August; Nobuakira Takeda; Atsushi Takeda; Markus Wilhelm; Mario C Deng; Hideo A Baba
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of pathology     Volume:  197     ISSN:  0022-3417     ISO Abbreviation:  J. Pathol.     Publication Date:  2002 Jun 
Date Detail:
Created Date:  2002-05-23     Completed Date:  2002-07-01     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0204634     Medline TA:  J Pathol     Country:  England    
Other Details:
Languages:  eng     Pagination:  230-7     Citation Subset:  IM    
Copyright Information:
Copyright 2002 John Wiley & Sons, Ltd.
Affiliation:
Institute of Pathology, University of Essen, Essen, Germany.
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MeSH Terms
Descriptor/Qualifier:
Adult
Animals
Anoxia / enzymology*
Cell Hypoxia / physiology
Cells, Cultured
Endothelium, Vascular / enzymology
Female
Heart Failure / enzymology*,  therapy
Heart-Assist Devices*
Heme Oxygenase (Decyclizing) / metabolism*
Heme Oxygenase-1
Humans
Male
Membrane Proteins
Middle Aged
Muscle, Smooth, Vascular / enzymology
Myocardium / enzymology*
Rats
Rats, Sprague-Dawley
Chemical
Reg. No./Substance:
0/Membrane Proteins; EC 1.14.99.3/HMOX1 protein, human; EC 1.14.99.3/Heme Oxygenase (Decyclizing); EC 1.14.99.3/Heme Oxygenase-1

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