CARDIOVASCULAR JOURNAL OF AFRICA • Volume 33, No 5, September/October 2022 232 AFRICA Javier et al. reported, for the first time, that several members of the small leucine-rich proteoglycan family, including asporin and PRELP, contribute to cardiac re-modelling.24 Bengtsson et al. showed that PRELP was an important regulator of cell adhesion, due to the positively charged N-terminal region in its chemical structure.24,25 Fibroblasts can adhere to PRELP and that can be inhibited by heparin.26 However, little research on PRELP’s role in myocardial fibrosis and ventricular re-modelling following AMI has been done. Our study determined the role of PRELP in myocardial fibrosis and re-modelling post AMI. Li et al. reported PRELP promotes osteoblastic differentiation via the β-catenin/connexin 43 pathway, and β-catenin acts as a hub gene in the PRELP gene network.5 Some studies showed that expression of the wnt pathway increased following AMI, and appropriate activation of the wnt pathway can decrease the infarct size of the heart and alleviate heart failure, while excess activation can lead to myocardial fibrosis.16,17 Other studies also noted that the wnt/β– catenin signalling pathway is involved in myocardial fibrosis post MI.27-31 However, there was no research until now that looked at PRELP’s role in myocardial fibrosis through the wnt/β–catenin signalling pathway post AMI. Conclusion Our study has shown for the first time that PRELP takes part in cardiac myofibrosis and ventricular re-modelling following AMI through the wnt/β–catenin signalling pathway. It further identified the cardiac fibrotic molecular mechanisms, provided novel insights into therapeutic targets and uncovered effective strategies to alleviate myocardial fibrosis after AMI. This study was supported by Natural Science Foundation of Shandong Province (ZR2017MH122). Fig. 3. PRELP promoted myocardial fibrosis and cardiac dysfunction after MI on the wnt/β–catenin signalling pathway. A and B. The expression levels of wnt1, GSK3β, MMP9, β-catenin, c-myc and TIMP-1 in myocardial tissues were detected using Western blotting; GAPDH was used as a loading control in these experiments. Data are shown as mean ± SEM. C and D. The expression levels of wnt1, GSK3β, MMP9, β-catenin, c-myc and TIMP-1 in fibroblasts were detected using Western blotting; GAPDH was used as a loading control in these experiments. Data are shown as mean ± SEM. E–G. The expression levels of GSK3β, wnt1 and β-catenin in fibroblasts were detected using immunohistochemical staining analysis. *p < 0.05, **p < 0.01, ***p < 0.001 versus the control group; #p < 0.05; ##p < 0.01; ###p < 0.001 versus the MI group.
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