RGD Reference Report - Cardiac myofibroblast differentiation is attenuated by alpha(3) integrin blockade: potential role in post-MI remodeling. - Rat Genome Database

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Cardiac myofibroblast differentiation is attenuated by alpha(3) integrin blockade: potential role in post-MI remodeling.

Authors: Bryant, JE  Shamhart, PE  Luther, DJ  Olson, ER  Koshy, JC  Costic, DJ  Mohile, MV  Dockry, M  Doane, KJ  Meszaros, JG 
Citation: Bryant JE, etal., J Mol Cell Cardiol. 2009 Feb;46(2):186-92. Epub 2008 Nov 7.
RGD ID: 2325287
Pubmed: PMID:19041328   (View Abstract at PubMed)
DOI: DOI:10.1016/j.yjmcc.2008.10.022   (Journal Full-text)

Cardiac fibroblasts and myofibroblasts are responsible for post-MI remodeling which occurs via regulation of extracellular matrix (ECM). Accelerated post-MI remodeling leads to excessive ECM deposition and fibrosis, contributing to impaired contractile function, arrhythmias, and heart failure. We have previously reported that type VI collagen induces myofibroblast differentiation in cultured cardiac fibroblasts, and that type VI collagen and myofibroblast content were both elevated in the myocardium 20 weeks post-MI. The purpose of this study was to determine the expression patterns of type VI collagen and myofibroblast content in early post-myocardial infarction (MI) remodeling to gain insight into whether type VI collagen induces in vivo myofibroblast differentiation via specific matrix-receptor interactions. Adult male Sprague-Dawley rats were anesthetized and left coronary arteries were permanently ligated. Histological tissue sections and whole tissue protein lysates were obtained from infarcted and non-infarcted areas of MI hearts and sham operated controls. At 3 days post-MI, we observed a significant increase in alpha(3) integrin expression (2.02+/-0.18 fold); at 7 days post-infarction both type VI collagen (2.27+/-0.18 fold) and myofibroblast (4.65+/-0.6 fold) content increased. By 14 days myofibroblast content returned to sham control levels, although type VI collagen (2.42+/-0.11 fold) was still elevated. In vitro cross-linking confirmed that the alpha(3) integrin interacts with type VI collagen, and alpha(3) integrin function blocking antibodies inhibited the differentiation of isolated cardiac fibroblasts. Collectively, our in vitro results indicate that the alpha(3) integrin receptor interacts with type VI collagen to promote myofibroblast differentiation, and that this interaction may impact in vivo post-MI remodeling.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
ITGA3Humanmyocardial infarction  ISOItga3 (Rattus norvegicus)protein:increased expression:myocardium (rat)RGD 
Itga3Ratmyocardial infarction  IEP protein:increased expression:myocardium (rat)RGD 
Itga3Mousemyocardial infarction  ISOItga3 (Rattus norvegicus)protein:increased expression:myocardium (rat)RGD 

Objects Annotated

Genes (Rattus norvegicus)
Itga3  (integrin subunit alpha 3)

Genes (Mus musculus)
Itga3  (integrin alpha 3)

Genes (Homo sapiens)
ITGA3  (integrin subunit alpha 3)


Additional Information