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Fibroblast growth factor‐2 inhibits CD40‐mediated periodontal inflammation
Author(s) -
Fujihara Chiharu,
Kanai Yu,
Masumoto Risa,
Kitagaki Jirouta,
Matsumoto Masahiro,
Yamada Satoru,
Kajikawa Tetsuhiro,
Murakami Shinya
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.27469
Subject(s) - inflammation , fibroblast growth factor , periodontal fiber , tumor necrosis factor alpha , regeneration (biology) , fibroblast , wound healing , microbiology and biotechnology , growth factor , transforming growth factor , immunology , cancer research , chemistry , medicine , biology , dentistry , in vitro , receptor , biochemistry
Fibroblast growth factor‐2 (FGF‐2) stimulates periodontal regeneration by a broad spectrum of effects on periodontal ligament (PDL) cells, such as proliferation, migration, and production of extracellular matrix. A critical factor in the success of periodontal regeneration is the rapid resolution of inflammatory responses in the tissue. We explored an anti‐inflammatory effect of FGF‐2 during periodontal regeneration and healing. We found that FGF‐2 on mouse periodontal ligament cells (MPDL22) markedly downregulated CD40 expression, a key player of inflammation. In addition, FGF‐2 inhibited CD40 signaling by the non‐canonical nuclear factor‐kappa B2 (NFκB2) pathway, resulting in decreased production of interleukin‐6 (IL‐6) and tumor necrosis factor‐α (TNF‐α), which have the potential to recruit immune cells to inflamed sites. Furthermore, in vivo treatment of FGF‐2 enhanced healing of skin wounds by counteracting the CD40‐mediated inflammation. These results reveal that FGF‐2 has an important function as a negative regulator of inflammation during periodontal regeneration and healing.