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Article has an altmetric score of 3

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Referenced in 1 patents
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Research Article Free access | 10.1172/JCI115685

Rapid expression of fibronectin in the rabbit heart after myocardial infarction with and without reperfusion.

A A Knowlton, C M Connelly, G M Romo, W Mamuya, C S Apstein, and P Brecher

Biochemistry Department, Whitaker Cardiovascular Institute, Boston University School of Medicine, Massachusetts 02118.

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Biochemistry Department, Whitaker Cardiovascular Institute, Boston University School of Medicine, Massachusetts 02118.

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Biochemistry Department, Whitaker Cardiovascular Institute, Boston University School of Medicine, Massachusetts 02118.

Find articles by Romo, G. in: JCI | PubMed | Google Scholar

Biochemistry Department, Whitaker Cardiovascular Institute, Boston University School of Medicine, Massachusetts 02118.

Find articles by Mamuya, W. in: JCI | PubMed | Google Scholar

Biochemistry Department, Whitaker Cardiovascular Institute, Boston University School of Medicine, Massachusetts 02118.

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Biochemistry Department, Whitaker Cardiovascular Institute, Boston University School of Medicine, Massachusetts 02118.

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Published April 1, 1992 - More info

Published in Volume 89, Issue 4 on April 1, 1992
J Clin Invest. 1992;89(4):1060–1068. https://doi.org/10.1172/JCI115685.
© 1992 The American Society for Clinical Investigation
Published April 1, 1992 - Version history
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Abstract

The expression of fibronectin in the repair process after myocardial infarction was studied using two protocols of coronary occlusion in the rabbit: a permanent occlusion or 3 h of occlusion followed by reperfusion (too late for salvage). We found a rapid and progressive increase in cardiac fibronectin expression in the infarcted region of the ventricle. Steady-state mRNA levels for fibronectin increased 13- and 16-fold, respectively, in the permanent and reperfused infarcts 1 d postinfarction. Immunological detection of the protein with a polyclonal antibody against plasma fibronectin showed significant increases of the protein fibronectin in the infarcted myocardium by day 3 in the reperfused group and by day 5 in the permanent coronary occlusion group. Ribonuclease protection assays established the induction of EIIIB containing fibronectin mRNA in both models by day 1 and use of a monoclonal antibody showed an increase in the EIIIA isoform 2 d postinfarction. Increases in steady-state mRNA levels for several collagen types were found in both groups, but these changes occurred after those noted for fibronectin. Thus fibronectin mRNA and protein expression increased rapidly postinfarction suggesting a functional role in the repair process.

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Referenced in 1 patents
38 readers on Mendeley
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