CARDIOVASCULAR JOURNAL OF AFRICA • Volume 33, No 5, September/October 2022 AFRICA 231 detect the expression levels of the above proteins of the wnt/β– catenin signalling pathway. Western blotting and immunohistochemical staining analysis showed that the expression levels of wnt1, GSK3β, MMP9, β-catenin, c-myc and TIMP-1 in the myocardial tissues and fibroblasts were more increased in PRELP over-expression groups than in the MI groups (Fig. 3). The expression levels of the above proteins in the sh-PRELP groups were decreased compared to the MI groups, indicating that PRELP increased the infarct size and promoted myocardial fibrosis and ventricular re-modelling following MI through the wnt/β–catenin signalling pathway in vivo and in vitro. Discussion In our study, we investigated the role of PRELP in ventricular re-modelling and myocardial fibrosis post AMI and explored the underlying mechanism through which PRELP brings about these changes. In our experiments, over-expression of PRELP increased the infarct size and myocardial fibrosis, and decreased the LVFS and LVEF of the heart, compared to the MI groups. By contrast, in the sh-PRELP group, there was a decrease in the infarct size and myocardial fibrosis, and an increase in LVFS and LVEF of the heart, compared to the MI groups. The results indicate that PRELP increased the infarct area and myocardial fibrosis and reduced the cardiac function post MI. The expression of wnt1, GSK3β, MMP9, β-catenin, c-myc and TIMP-1 was greater in the group with over-expression of PRELP than in the MI groups, both in vivo and in vitro. The expression of these proteins in sh-PRELP groups was lower than that in the MI groups. The results indicate that PRELP takes part in myocardial fibrosis and ventricular re-modelling post AMI through the wnt/β–catenin signalling pathway. Several previous studies have shown that other members of the SLRR family such as biglycan, glypican-6 and lumican take part in myocardial fibrosis and ventricular re-modelling.10-12,22,23 Fig. 2. PRELP increased the infarct size and myocardial fibrosis promoted cardiac dysfunction after MI. A. Representative echocardiographic M-mode images of left ventricles from SHAM, MI, MI + PRELP shRNA and MI + PRELP over groups. B. Echocardiographic measurement of LVEF and LVFS in mice in the four groups. C and D. Representative images of heart sections stained with TTC from mice in the four groups; the infarct size (white area) was measured and shown as a percentage of the total section area of the left ventricular myocardium. E–G. Representative images of heart sections stained with haematoxylin and eosin (E) and Sirius red (F and G); F was for myocardial tissues and G was for fibroblasts in the four groups.
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