Fibroblast growth factor‐2 inhibits CD40‐mediated periodontal inflammation

Fujihara, Chiharu; Kanai, Yu; Masumoto, Risa; Kitagaki, Jirouta; Matsumoto, Masahiro; Yamada, Satoru; Kajikawa, Tetsuhiro; Murakami, Shinya

doi:10.1002/jcp.27469

Cited by 17 publications

(12 citation statements)

References 38 publications

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“…As a well-known growth factor, bFGF regulates the proliferation, apoptosis, and regeneration of several cells/tissues, including gingiva and periodontal ligament [96,97]. More recently, it was reported that bFGF inhibits periodontal inflammation by suppressing CD40-mediated inflammatory signaling [98]. Based on the regenerative capacity of bFGF, many clinical trials were already performed to recuperate periodontal tissue which was disrupted by age or pathological conditions.…”

Section: Othersmentioning

confidence: 99%

Effect of Aging on Homeostasis in the Soft Tissue of the Periodontium: A Narrative Review

Kim

Lee

Bae

et al. 2021

JPM

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Aging is characterized by a progressive decline or loss of physiological functions, leading to increased susceptibility to disease or death. Several aging hallmarks, including genomic instability, cellular senescence, and mitochondrial dysfunction, have been suggested, which often lead to the numerous aging disorders. The periodontium, a complex structure surrounding and supporting the teeth, is composed of the gingiva, periodontal ligament, cementum, and alveolar bone. Supportive and protective roles of the periodontium are very critical to sustain life, but the periodontium undergoes morphological and physiological changes with age. In this review, we summarize the current knowledge of molecular and cellular physiological changes in the periodontium, by focusing on soft tissues including gingiva and periodontal ligament.

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Section: Othersmentioning

confidence: 99%

Effect of Aging on Homeostasis in the Soft Tissue of the Periodontium: A Narrative Review

Kim

Lee

Bae

et al. 2021

JPM

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“…FGF2 is the most studied growth factor of the FGF family that is expressed in many tissues and body fluids, including the tears and saliva [ 29 ]. It induces periodontal regeneration and suppresses inflammation indicating its role in regeneration and healing [ 30 ]. In this study, FGF5 was also identified, which has the same effect on growth/differentiation balance of PDL cells, and is expressed in large amounts in PDL cell culture [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

Identification of bone morphogenetic protein 4 in the saliva after the placement of fixed orthodontic appliance

et al. 2021

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Background This study was conducted in order to explore the effects of orthodontic tooth movement (OTM) on the changes of salivary proteome. This prospective observational pilot study recruited 12 healthy teenage boys with malocclusion treated with a fixed orthodontic appliance and 6 appropriate control participants. Saliva samples were collected a day before and at 0, 2, 7, and 30 days after initialization of treatment, corresponding to the initial, lag, and post-lag phases of OTM. Pooled samples were analyzed by liquid chromatography-mass spectrometry, ELISA, and Western blotting. To date, there is no published data on the presence of BMP molecules or their antagonists in the saliva or in the gingival cervical fluid related to orthodontic conditions. Results A total of 198 identified saliva proteins were classified based on their functional characteristics. Proteins involved in bone remodeling were observed exclusively 30 days post appliance placement, including bone morphogenetic protein 4 (BMP4), a BMP antagonist BMP-binding endothelial regulator, insulin-like growth factor-binding protein 3, cytoskeleton-associated protein 4, and fibroblast growth factor 5. Based on the analysis of protein interactions, BMP4 was found to have a central position in this OTM-related protein network. Conclusions The placement of a fixed orthodontic appliance induced occurrence of proteins involved in bone remodeling in the saliva at a time corresponding to the post-lag period of OTM. Limitations of this study include a relatively small sample size, limited time of monitoring patients, and the lack of interindividual variability assessment.

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“…Activation of FGF signalling by exogenous FGF2 may regulate NF-kB because of the suppressive effect of FGF2 on inflammation (22). Thus, we investigated the relationship between phosphorylated RelA and FGF2 stimulation.…”

Section: Discussionmentioning

confidence: 99%

Regulation of NF-kB Signalling Through the PR55β-RelA Interaction in Osteoblasts

Suzuki

Sugiyama

Ohyama

et al. 2020

In Vivo

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Background/Aim: Nuclear factor kappa B (NF-kB) signalling including the RelA subunit is activated upon fibroblast growth factor (FGF) stimulation. A clear understanding of the mechanisms underlying this action will provide insights into molecular targeting therapy. Furthermore, protein phosphatase 2A (PP2A) is involved in RelA dephosphorylation, but little is known about the underlying mechanism. Materials and Methods: Because the regulatory subunits of PP2A drive NF-kB signalling via RelA, we used qRT-PCR and immunoblot analysis to investigate the expression of these subunits in MC3T3-E1 cells. We examined weather FGF2 interacts with NF-kB using immunocytochemistry (IC), immunoprecipitation (IP), and pull-down assay (PD) using recombinant proteins. Results: PR55β expression was increased, whereas activated RelA was dephosphorylated upon FGF2 stimulation. Further, the interaction of PR55β with RelA was confirmed by IC, IP, and PD. Conclusion: FGF2-induced PR55β directly interacts with RelA and regulates NF-kB signalling.

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Fibroblast growth factor‐2 inhibits CD40‐mediated periodontal inflammation

Cited by 17 publications

References 38 publications

Effect of Aging on Homeostasis in the Soft Tissue of the Periodontium: A Narrative Review

Effect of Aging on Homeostasis in the Soft Tissue of the Periodontium: A Narrative Review

Identification of bone morphogenetic protein 4 in the saliva after the placement of fixed orthodontic appliance

Regulation of NF-kB Signalling Through the PR55β-RelA Interaction in Osteoblasts

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