Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/9941
Title: Connective tissue growth factor and cardiac fibrosis after myocardial infarction.
Authors: Dean, Rachael G;Balding, Leanne C;Candido, Riccardo;Burns, Wendy C;Cao, Zemin;Twigg, Stephen M;Burrell, Louise M
Affiliation: Department of Medicine, Austin Health, The University of Melbourne, Heidelberg, Victoria, Australia
rdean@unimelb.edu.au
Issue Date: 13-Jun-2005
Citation: The Journal of Histochemistry and Cytochemistry : Official Journal of the Histochemistry Society 2005; 53(10): 1245-56
Abstract: The temporal and spatial expression of transforming growth factor (TGF)-beta(1) and connective tissue growth factor (CTGF) was assessed in the left ventricle of a myocardial infarction (MI) model of injury with and without angiotensin-converting enzyme (ACE) inhibition. Coronary artery ligated rats were killed 1, 3, 7, 28, and 180 days after MI. TGF-beta(1), CTGF, and procollagen alpha1(I) mRNA were localized by in situ hybridization, and TGF-beta(1) and CTGF protein levels by immunohistochemistry. Collagen protein was measured using picrosirius red staining. In a separate group, rats were treated for 6 months with an ACE inhibitor. There were temporal and regional differences in the expression of TGF-beta(1), CTGF, and collagen after MI. Procollagen alpha1(I) mRNA expression increased in the border zone and scar peaking 1 week after MI, whereas collagen protein increased in all areas of the heart over the 180 days. Expression of TGF-beta(1) mRNA and protein showed major increases in the border zone and scar peaking 1 week after MI. The major increases in CTGF mRNA and protein occurred in the viable myocardium at 180 days after MI. Long-term ACE inhibition reduced left ventricular mass and decreased fibrosis in the viable myocardium, but had no effect on cardiac TGF-beta(1) or CTGF. TGF-beta(1) is involved in the initial, acute phase of inflammation and repair after MI, whereas CTGF is involved in the ongoing fibrosis of the heart. The antifibrotic benefits of captopril are not mediated through a reduction in CTGF.
Internal ID Number: 15956033
URI: http://ahro.austin.org.au/austinjspui/handle/1/9941
DOI: 10.1369/jhc.4A6560.2005
URL: http://www.ncbi.nlm.nih.gov/pubmed/15956033
Type: Journal Article
Subjects: Angiotensin-Converting Enzyme Inhibitors.pharmacology
Animals
Captopril.pharmacology
Collagen Type I.biosynthesis
Connective Tissue Growth Factor
Fibrosis
Immediate-Early Proteins.biosynthesis
Immunohistochemistry
In Situ Hybridization
Intercellular Signaling Peptides and Proteins.biosynthesis
Myocardial Infarction.metabolism.pathology
Myocardium.metabolism.pathology
Myocytes, Cardiac.metabolism
RNA, Messenger.biosynthesis
Rats
Time Factors
Transforming Growth Factor beta.biosynthesis
Transforming Growth Factor beta1
Ventricular Remodeling
Appears in Collections:Journal articles

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