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

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.

SUBMITTER: He T

PROVIDER: S-EPMC5722540 | biostudies-literature | 2017 Nov

REPOSITORIES: biostudies-literature

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

He Tao T Huang Yan Y Zhang Chen C Liu Denghui D Cheng Chao C Xu Weidong W Zhang Xiaoling X

Oncotarget 20170911 57

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 ...[more]

PMID: 29228588

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