Scleraxis and transcription factor 15 expression in the failing myocardium
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There is still no specific treatment for fibrosis, a common co-morbidity to many cardiovascular diseases. We examined the association in expression of the pro-fibrotic protein scleraxis and its paralog transcription factor 15 (TCF15), with the myofibroblast marker α-smooth muscle actin (α-SMA), after myocardial infarction (MI) in an experimental model in vivo. Echocardiography revealed that the hearts of the post-infarct rats were in a state of systolic dysfunction across all time points. Left (infarcted scar and non-infarcted) and right cardiac ventricles from male Sprague-Dawley rats were obtained at 2-4 days and 1-8 weeks post-MI. Western blot analysis shows that scleraxis, TCF15 and α-SMA is all increased within the infarct scar in all stages of wound healing compared to sham-operated controls. Thus, scleraxis and TCF15 are co-expressed in the infarct scar of post-MI hearts. Using one of these proteins as a biological target for possible treatments may serve to limit cardiac fibrosis.