Interleukin-17A-promoted MSC2 polarization related with new bone formation of ankylosing spondylitis
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Tao He1,*, Yan Huang2,*, Chen Zhang1, Denghui Liu1, Chao Cheng4, Weidong Xu1 and Xiaoling Zhang2,3
1Department of Joint Surgery and Sports Medicine, Changhai Hospital Affiliated to the Second Military Medical University, Shanghai, People’s Republic of China
2The Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Jiao Tong University School of Medicine, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, People’s Republic of China
3Department of Orthopedic Surgery, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, People’s Republic of China
4Department of Nuclear Medicine, Changhai Hospital Affiliated to the Second Military Medical University, Shanghai, People’s Republic of China
*These authors contributed equally to this work
Weidong Xu, email: firstname.lastname@example.org
Xiaoling Zhang, email: email@example.com
Keywords: interleukin-17, mesenchymal stem cells, polarization, new bone formation, ankylosing spondylitis
Received: July 21, 2017 Accepted: August 19, 2017 Published: September 11, 2017
It’s still unknown how over-hyperplasia of tissue such like new bone formation (NBF) developed in ankylosing spondylitis (AS). We found low level of IL-17A promoted TLR4+MSC1 polarization with suppressed osteogenic differentiation through JAK2/STAT3 pathway, while high level of IL-17A promoted TLR3+MSC2 polarization with enhanced osteogenic differentiation through WNT10b/RUNX2 pathway. Furthermore, both proteoglycan-induced spondylitis (PGISp) mouse model and AS patients without NBF showed MSC1 polarization, up-regulated JAK2/STAT3 pathway and high level of IL-17A (peripherally, but not locally), but those with NBF showed MSC2 polarization, up-regulated WNT10b/RUNX2 pathway and high expression of IL-17A at local site. Results showed NBF of AS was induced by MSC2 polarization that was promoted by high level of IL-17A, and may be treated by suppressing local MSC2 polarization.
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