Document Detail

Long-term therapy with the acorn cardiac support device normalizes gene expression of growth factors and gelatinases in dogs with heart failure.
MedLine Citation:
PMID:  16210139     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: Passive mechanical containment of the failing left ventricle with the Acorn Cardiac Support Device (CSD) was shown to prevent progressive left ventricular dilation in dogs with heart failure and increase left ventricular ejection fraction. To examine possible mechanisms for improved cardiac function with a CSD, we examined the effect of CSD therapy on the mRNA gene expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), matrix metalloproteinases (MMP) 2 and 9, and tissue inhibitors of metalloproteinases (TIMP) 1 and 2. METHODS: Heart failure was produced in 12 dogs by multiple sequential intracoronary microembolizations. Six dogs were implanted with the CSD and 6 served as concurrent controls. Left ventricular tissue from 6 normal dogs was used for comparison. RESULTS: Compared with normal dogs, dogs with untreated heart failure showed downregulation of mRNA expression for VEGF and bFGF, whereas upregulation of mRNA expression for MMP-2 and MMP-9 was observed. Normalization of mRNA expression for all these genes was seen after treatment with the CSD. CONCLUSIONS: This study shows that preventing left ventricular dilation and myocardial stretch with the CSD promotes normalization of growth factor and MMP gene expression. These results suggest that modulation of gene activity may, in part, contribute to the improvement of left ventricular function observed with CSD therapy.
Sharad Rastogi; Ramesh C Gupta; Sudhish Mishra; Hideaki Morita; Elaine J Tanhehco; Hani N Sabbah
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation     Volume:  24     ISSN:  1557-3117     ISO Abbreviation:  J. Heart Lung Transplant.     Publication Date:  2005 Oct 
Date Detail:
Created Date:  2005-10-07     Completed Date:  2006-07-06     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  9102703     Medline TA:  J Heart Lung Transplant     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1619-25     Citation Subset:  IM    
Division of Cardiovascular Medicine, Department of Medicine, Henry Ford Heart and Vascular Institute, Detroit, Michigan 48202-2689, USA.
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MeSH Terms
Dilatation, Pathologic / etiology,  therapy*
Disease Models, Animal
Disease Progression
Fibroblast Growth Factor 2 / analysis,  biosynthesis
Gene Expression
Gene Expression Regulation
Heart Catheterization
Heart Failure / complications,  therapy*
Matrix Metalloproteinase 2 / analysis,  biosynthesis
Prosthesis Implantation*
RNA, Messenger / biosynthesis
Sequence Analysis, DNA
Stroke Volume
Surgical Mesh*
Tissue Inhibitor of Metalloproteinase-1 / analysis,  biosynthesis
Tissue Inhibitor of Metalloproteinase-2 / analysis,  biosynthesis
Vascular Endothelial Growth Factor A / analysis,  biosynthesis
Ventricular Dysfunction, Left / etiology,  therapy*
Grant Support
Reg. No./Substance:
0/RNA, Messenger; 0/Tissue Inhibitor of Metalloproteinase-1; 0/Vascular Endothelial Growth Factor A; 103107-01-3/Fibroblast Growth Factor 2; 127497-59-0/Tissue Inhibitor of Metalloproteinase-2; EC Metalloproteinase 2

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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