Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1999-7-8
pubmed:abstractText
We have previously shown that non-myocytes present in healed 8-week infarct scar overexpress transduction proteins required for initiating the elevated deposition of structural matrix proteins in this tissue. Other work suggests that TGF-beta 1 may be involved in cardiac fibrosis and myocyte hypertrophy. However, the significance of the altered TGF-beta signaling in heart failure in the chronic phase of post-myocardial infarction (MI), particularly in the ongoing remodeling of the infarct scar, remains unexplored. Patterns of cardiac TGF beta 1 and Smad 2, 3, and 4 protein expression were investigated 8 weeks after MI and were compared to relative collagen deposition in border tissues (containing remnent myocytes) and the infarct scar (non-myocytes). Both TGF-beta 1 mRNA abundance and protein levels were significantly increased in the infarct scar v control values, and this trend was positively correlated to increased collagen type I expression. Cardiac Smad 2, 3, and 4 proteins were significantly increased in border and scar tissues v control values. Immunofluorescent studies indicated that Smad proteins localized proximal to the cellular nuclei present in the infarct scar. Decorin mRNA abundance was elevated in border and infarct scar, and the pattern of decorin immunostaining was markedly altered in remote remnant heart and scar v staining patterns of control sections. Expression of T beta RI (53 kDa) protein was significantly reduced in the scar, while the 75 kDa and 110 kDa isoforms of T beta RII were unchanged and significantly increased in scar, respectively. These results indicate that TGF-beta/Smad signaling may be involved in the remodeling of the infarct scar after the completion of wound healing per se, via ongoing stimulation of matrix deposition.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Activin Receptors, Type I, http://linkedlifedata.com/resource/pubmed/chemical/Collagen, http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Dcn protein, rat, http://linkedlifedata.com/resource/pubmed/chemical/Decorin, http://linkedlifedata.com/resource/pubmed/chemical/Extracellular Matrix Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Madh2 protein, rat, http://linkedlifedata.com/resource/pubmed/chemical/Madh3 protein, rat, http://linkedlifedata.com/resource/pubmed/chemical/Madh4 protein, rat, http://linkedlifedata.com/resource/pubmed/chemical/Protein-Serine-Threonine Kinases, http://linkedlifedata.com/resource/pubmed/chemical/Proteoglycans, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Transforming Growth..., http://linkedlifedata.com/resource/pubmed/chemical/Smad2 Protein, http://linkedlifedata.com/resource/pubmed/chemical/Smad3 Protein, http://linkedlifedata.com/resource/pubmed/chemical/Smad4 Protein, http://linkedlifedata.com/resource/pubmed/chemical/TGF-beta type I receptor, http://linkedlifedata.com/resource/pubmed/chemical/Trans-Activators, http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta, http://linkedlifedata.com/resource/pubmed/chemical/transforming growth factor-beta...
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0022-2828
pubmed:author
pubmed:issnType
Print
pubmed:volume
31
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
667-78
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:10198196-Activin Receptors, Type I, pubmed-meshheading:10198196-Animals, pubmed-meshheading:10198196-Blotting, Western, pubmed-meshheading:10198196-Cicatrix, pubmed-meshheading:10198196-Collagen, pubmed-meshheading:10198196-DNA-Binding Proteins, pubmed-meshheading:10198196-Decorin, pubmed-meshheading:10198196-Disease Models, Animal, pubmed-meshheading:10198196-Enzyme-Linked Immunosorbent Assay, pubmed-meshheading:10198196-Extracellular Matrix Proteins, pubmed-meshheading:10198196-Fluorescent Antibody Technique, pubmed-meshheading:10198196-Heart, pubmed-meshheading:10198196-Hemodynamics, pubmed-meshheading:10198196-Male, pubmed-meshheading:10198196-Myocardial Infarction, pubmed-meshheading:10198196-Myocardium, pubmed-meshheading:10198196-Protein-Serine-Threonine Kinases, pubmed-meshheading:10198196-Proteoglycans, pubmed-meshheading:10198196-Rats, pubmed-meshheading:10198196-Rats, Sprague-Dawley, pubmed-meshheading:10198196-Receptors, Transforming Growth Factor beta, pubmed-meshheading:10198196-Smad2 Protein, pubmed-meshheading:10198196-Smad3 Protein, pubmed-meshheading:10198196-Smad4 Protein, pubmed-meshheading:10198196-Trans-Activators, pubmed-meshheading:10198196-Transforming Growth Factor beta
pubmed:year
1999
pubmed:articleTitle
Elevation of expression of Smads 2, 3, and 4, decorin and TGF-beta in the chronic phase of myocardial infarct scar healing.
pubmed:affiliation
Laboratory of Molecular Cardiology, St. Boniface General Hospital Research Centre, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't