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HDAC10 upregulation contributes to interleukin 1β‐mediated inflammatory activation of synovium‐derived mesenchymal stem cells in temporomandibular joint
Author(s) -
Liao Wenting,
Sun Jiadong,
Liu Wenjing,
Li Wenyu,
Jia Jiaxin,
Ou Farong,
Su Kai,
Zheng Youhua,
Zhang Zhiguang,
Sun Yangpeng
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.27873
Subject(s) - mesenchymal stem cell , downregulation and upregulation , temporomandibular joint , inflammation , medicine , microbiology and biotechnology , orthodontics , biology , immunology , pathology , genetics , gene
Histone deacetylases (HDACs) are important in chronic inflammation, and inflammatory responses affect synovium‐derived mesenchymal stem cell (SMSC) function in temporomandibular joint repair. However, the effect of HDACs on SMSC inflammatory activation remains unclear. In this study, temporomandibular joint fibroblast‐like synoviocytes obtained from osteoarthritis patients met the minimal mesenchymal stem cell criteria. Interleukin 1β (IL‐1β) upregulated IL‐6 and IL‐8 expression in SMSCs through nuclear factor‐κB (NF‐κB) pathway activation. IL‐6 and IL‐8 upregulation were blocked by broad‐acting HDAC inhibitors SAHA and LBH589. MC1568 alleviated IL‐1β activation of SMSCs, whereas CI994 and FK228 produced a minimal or opposite effect in vitro. We also found HDAC10 was highly associated with localized IL‐1β expression in vivo and in vitro. HDAC10 knockdown alleviated IL‐1β‐mediated SMSC activation and blocked NF‐κB pathway activation. Conversely, HDAC10 overexpression promoted IL‐6 and IL‐8 expression and IL‐1β‐mediated NF‐κB pathway activation. In conclusion, HDAC10 upregulation contributed to IL‐1β‐mediated inflammatory activation of SMSCs, indicating that HDAC10 may be a novel therapeutic target.