Abstract
Due to the complex nature of the tendon architecture, the regeneration of these tissues results in the formation of scars. As a direct result of scar formation, the ability of the tendon tissues to function is impaired and often results in further damage that has been afflicted to the tendon architecture. The growth and proliferation of tendon fibroblasts involve a complex network of signalling molecules. To understand and aid in the proper repair of this complex tissue network, a more in-depth understanding is required in the events that induce the growth of tendon cells. Several studies have shown the apoptotic mechanisms induced by the mitogen, hepatocyte growth factor, in multiple biological and pathological systems. In our recent research, we have described a mechanism where hepatocyte growth factor (HGF) is able to inhibit the proliferative effects of transforming growth factor-β1 (TGF-β1) and induce apoptosis in rat tendon fibroblasts. Transforming growth factor-β1 is able to induce the proliferation of fibroblast cells by increasing both the gene expression and protein levels of α-smooth muscle actin (α-SMA) and c-MET. We have also shown that inhibition of extracellular signal-regulated kinase 1/2 does not block hepatocyte growth factor-induced growth arrest. However, we have shown that blocking the activity of focal adhesion kinase can prevent the growth inhibition ability of hepatocyte growth factor in tendon fibroblasts. Collectively, our studies show growth inhibitory pathway in tendon fibroblasts induced by hepatocyte growth factor and mediated focal adhesion kinase.
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Acknowledgments
This work was supported by grants from the National Natural Sciences Foundation of China (Nos. 81272049 and 81150024), the Natural Science Foundation of Heilongjiang Province (D201007), the Scientific Research Foundation for the Returned Overseas of the Department of Science and Technology of Harbin (2010RFLXS009) and the Scientific Research Foundation of the Department of Education of Heilongjiang Province (12531378). Qingbo Cui is supported by the National Natural Sciences Foundation of China (Nos. 81101349).
We would also like to thank Professor Yuhui Xi and the School of Pathophysiology, Harbin Medical University for supporting the research project.
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Zhao, Z., Sun, Y., Yang, S. et al. FAK activity is required for HGF to suppress TGF-β1-induced cellular proliferation. In Vitro Cell.Dev.Biol.-Animal 51, 941–949 (2015). https://doi.org/10.1007/s11626-015-9914-y
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DOI: https://doi.org/10.1007/s11626-015-9914-y