Wnt3α and transforming growth factor-β induce myofibroblast differentiation from periodontal ligament cells via different pathways

Publication date: Available online 20 February 2017
Source:Experimental Cell Research
Author(s): Hui Xu, Yao He, Jian Q. Feng, Rui Shu, Zhe Liu, Jingyu Li, Yating Wang, Yang Xu, Huan Zeng, Xin Xu, Zichao Xiang, Chaoran Xue, Ding Bai, Xianglong Han
Myofibroblasts are specialized cells that play a key role in connective tissue remodeling and reconstruction. Alpha-smooth muscle actin (α-SMA), vimentin and tenascin-C are myofibroblast phenotype, while α-SMA is the phenotypic marker. The observation that human periodontal ligament cells (hPDLCs) differentiate into myofibroblasts under orthodontic force has provided a new perspective for understanding of the biological and biomechanical mechanisms involved in orthodontic tooth movement. However, the cell-specific molecular mechanisms leading to myofibroblast differentiation in the periodontal ligament (PDL) remain unclear. In this study, we found that expression of Wnt3α, transforming growth factor-β1 (TGF-β1), α-SMA and tenascin-C increased in both tension and compression regions of the PDL under orthodontic load compared with unloaded control, suggesting that upregulated Wnt3α and TGF-β1 signaling might have roles in myofibroblast differentiation in response to orthodontic force. We reveal in vitro that both Wnt3α and TGF-β1 promote myofibroblast differentiation from hPDLCs. Dickkopf-1 (DKK1) impairs Wnt3α-induced myofibroblast differentiation in a β-catenin-dependent manner. TGF-β1 stimulates myofibroblast differentiation via a JNK-dependent mechanism. DKK1 has no significant effect on TGF-β1-induced myofibroblastic phenotype.



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