Format

Send to

Choose Destination
Oncotarget. 2017 Sep 11;8(57):96993-97008. doi: 10.18632/oncotarget.20823. eCollection 2017 Nov 14.

Interleukin-17A-promoted MSC2 polarization related with new bone formation of ankylosing spondylitis.

Author information

1
Department of Joint Surgery and Sports Medicine, Changhai Hospital Affiliated to the Second Military Medical University, Shanghai, People's Republic of China.
2
The 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.
3
Department of Nuclear Medicine, Changhai Hospital Affiliated to the Second Military Medical University, Shanghai, People's Republic of China.
4
Department of Orthopedic Surgery, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, People's Republic of China.

Abstract

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.

KEYWORDS:

ankylosing spondylitis; interleukin-17; mesenchymal stem cells; new bone formation; polarization

Conflict of interest statement

CONFLICTS OF INTEREST The authors declare that they have no competing interests

Supplemental Content

Full text links

Icon for Impact Journals, LLC Icon for PubMed Central
Loading ...
Support Center