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Originally published as JHC exPRESS on June 13, 2005.
doi:10.1369/jhc.4A6560.2005
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Journal of Histochemistry and Cytochemistry
Volume 53 (10): 1245-1256, 2005
Copyright ©The Histochemical Society, Inc.

Connective Tissue Growth Factor and Cardiac Fibrosis after Myocardial Infarction

Rachael G. Dean, Leanne C. Balding, Riccardo Candido, Wendy C. Burns, Zemin Cao, Stephen M. Twigg and Louise M. Burrell

Department of Medicine, University of Melbourne, Austin Health, Heidelberg, Victoria, Australia (RGD,LCB,RC,ZC,LMB); Diabetic Complications Group, Baker Heart Research Institute, Prahan, Victoria, Australia (WCB); and Kolling Institute of Medical Research, University of Sydney, Royal North Shore Hospital, St. Leonards, New South Wales, Australia (SMT)

Correspondence to: Dr. Rachael Dean, Department of Medicine, University of Melbourne, Austin Health (Repat Campus), Heidelberg, 3081, Victoria, Australia. E-mail: rdean{at}unimelb.edu.au

The temporal and spatial expression of transforming growth factor (TGF)-ß1 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-ß1, CTGF, and procollagen {alpha}1(I) mRNA were localized by in situ hybridization, and TGF-ß1 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-ß1, CTGF, and collagen after MI. Procollagen {alpha}1(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-ß1 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-ß1 or CTGF. TGF-ß1 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.

(J Histochem Cytochem 53:1245–1256, 2005)

Key Words: connective tissue growth factor • transforming growth factor ß1 • myocardial infarction • fibrosis • angiotensin-converting enzyme


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