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Abstract
Endothelial to mesenchymal transition (EndMT) and myofibroblast differentiation (FibroMF) occur in embryogenesis and adult pathologies such as the organ fibrosis. Stromelysin1, a matrix metalloprotease-3 (MMP3) is another molecule that has been indicated in vascular injury and organ fibrosis. There is a gap in knowledge on the specific role of stromelysin1 either in EndMT or in FibroMF. The objective of the current master of science research dissertation was to investigate the role of stromelysin1 in TGF2-induced EndMT and TGF1-induced FibroM. In our results, TGF2 treatment of endothelial cells (ECs) induced EndMT and increased expression of stromelysin1 and mesenchymal markers. Inhibition of stromelysin1 blunted TGF2-induced EndMT. In contrast, treatment of NIH-3T3 fibroblasts with TGF1 promoted FibroMF. Intriguingly, stromelysin1 inhibition in TGF1-stimulated myofibroblasts further exacerbated fibroproliferation with increased FibroMF marker expression. In conclusion, our study has identified that EndMT and FibroMF are reciprocally regulated by stromelysin1.