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β-catenin activation in hair follicle dermal stem cells induces ectopic hair outgrowth and skin fibrosis Free
Yixin Tao 1,2 , Qingchun Yang2 , Lei Wang2 , Jie Zhang2 , Xuming Zhu2 , Qianqian Sun2 , Yunbin Han3 , Qian Luo3 , Yushu Wang2 , Xizhi Guo2 , Ji Wu2 , Baojie Li2 , Xiao Yang4 , Lin He 2,* , and Gang Ma 1,2,*
1 Bio-X-Renji Hospital Research Center, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200240, China
2 Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders (Ministry of Education), Bio-X Institutes, Shanghai Jiao Tong University, Shanghai 200240, China
3 School of Life Science and Biotechnology, Shanghai Jiao Tong University, Shanghai 200240, China
4 State Key Laboratory of Proteomics, Genetic Laboratory of Development and Diseases, Institute of Biotechnology,Beijing 100071, China *Correspondence to:Gang Ma, E-mail:, Lin He, E-mail:
J Mol Cell Biol, Volume 11, Issue 1, January 2019, Pages 26-38
Keyword: Wnt/β-catenin, fibrosis, hair follicle, skin, cell differentiation

Hair follicle dermal sheath (DS) harbors hair follicle dermal stem cells (hfDSCs), which can be recruited to replenish DS and dermal papilla (DP). Cultured DS cells can differentiate into various cell lineages in vitro. However, it is unclear how its plasticity is modulated in vivo. Wnt/β-catenin signaling plays an important role in maintaining stem cells of various lineages and is required for HF development and regeneration. Here we report that activation of β-catenin in DS generates ectopic HF outgrowth (EF) by reprogramming HF epidermal cells and DS cells themselves, and endows DS cells with hair inducing ability. Epidermal homeostasis of pre-existing HFs is disrupted. Additionally, cell-autonomous progressive skin fibrosis is prominent in dermis, where the excessive fibroblasts largely originate from DS. Gene expression analysis of purified DS cells with activated β-catenin revealed significantly increased expression of Bmp, Fgf, and Notch ligands and administration of Bmp, Fgf, or Notch signaling inhibitor attenuates EF formation. In summary, our findings advance the current knowledge of high plasticity of DS cells and provide an insight into understanding how Wnt/β-catenin signaling controls DS cell behaviors.