Linked Life Data

15840903

Source:http://linkedlifedata.com/resource/pubmed/id/15840903

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2005-4-20
pubmed:abstractText
Structural remodeling of the myocardium, including myocyte hypertrophy, myocardial fibrosis, and dilatation, drives functional impairment in various forms of acquired and hereditary cardiomyopathy. Using cardiomyopathic Syrian hamsters with a genetic defect in delta-sarcoglycan, we investigated the potential involvement of hepatocyte growth factor (HGF) in the pathophysiology and therapeutics related to dilated cardiomyopathy, because HGF has previously been shown to be cytoprotective and to have benefits in acute heart injury. Late-stage TO-2 cardiomyopathic hamsters showed severe cardiac dysfunction and fibrosis, accompanied by increases in myocardial expression of transforming growth factor-beta1 (TGF-beta1), a growth factor responsible for tissue fibrosis. Conversely, HGF was downregulated in late-stage myopathic hearts. Treatment with recombinant human HGF for 3 wk suppressed cardiac fibrosis, accompanied by a decreased expression of TGF-beta1 and type I collagen. Suppression of TGF-beta1 and type I collagen by HGF was also shown in cultured cardiac myofibroblasts. Likewise, HGF suppressed myocardial hypertrophy, apoptosis in cardiomyocytes, and expression of atrial natriuretic polypeptide, a molecular marker of hypertrophy. Importantly, downregulation of the fibrogenic and hypertrophic genes by HGF treatment was associated with improved cardiac function. Thus the decrease in endogenous HGF levels may participate in the susceptibility of cardiac tissue to hypertrophy and fibrosis, and exogenous HGF led to therapeutic benefits in case of dilated cardiomyopathy in this model, even at the late-stage treatment.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0363-6135
pubmed:author
pubmed:issnType
Print
pubmed:volume
288
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H2131-9
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:15840903-Angiotensin II, pubmed-meshheading:15840903-Animals, pubmed-meshheading:15840903-CHO Cells, pubmed-meshheading:15840903-Cardiomyopathy, Dilated, pubmed-meshheading:15840903-Cardiomyopathy, Hypertrophic, pubmed-meshheading:15840903-Cricetinae, pubmed-meshheading:15840903-Fibrosis, pubmed-meshheading:15840903-Gene Expression, pubmed-meshheading:15840903-Hepatocyte Growth Factor, pubmed-meshheading:15840903-Humans, pubmed-meshheading:15840903-Male, pubmed-meshheading:15840903-Mesocricetus, pubmed-meshheading:15840903-Myocytes, Cardiac, pubmed-meshheading:15840903-Proto-Oncogene Proteins c-met, pubmed-meshheading:15840903-Transforming Growth Factor beta, pubmed-meshheading:15840903-Transforming Growth Factor beta1, pubmed-meshheading:15840903-Vasoconstrictor Agents, pubmed-meshheading:15840903-Ventricular Remodeling
pubmed:year
2005
pubmed:articleTitle
Hepatocyte growth factor prevents tissue fibrosis, remodeling, and dysfunction in cardiomyopathic hamster hearts.
pubmed:affiliation
Division of Molecular Regenerative Medicine, Course of Advanced Medicine, Osaka University Graduate School of Medicine, Suita, Osaka, Japan. nakamura@onbich.med.osaka-u.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't