Regulation of Osteoclast Differentiation by Fibroblast Growth Factor 2: Stimulation of Receptor Activator of Nuclear Factor κB Ligand/Osteoclast Differentiation Factor Expression in Osteoblasts and Inhibition of Macrophage Colony-Stimulating Factor Function in Osteoclast Precursors

Chikazu, Daichi; Katagiri, Mika; Ogasawara, Toru; Ogata, Naoshi; Shimoaka, Takashi; Takato, Tsuyoshi; Nakamura, Kozo; Kawaguchi, Hiroshi

doi:10.1359/jbmr.2001.16.11.2074

Cited by 75 publications

(53 citation statements)

References 38 publications

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“…Some previous studies using β-TCP have reported the appearance of osteoclasts. This finding may conflict with previous evidence which demonstrated that bFGF-2 regulated osteoclast differentiation 35) . The osteoclasts on the surface of β-TCP in the TF group might have promoted the resorption of residual β-TCP in the furcation defect.…”

Section: Discussioncontrasting

confidence: 95%

Periodontal regeneration following application of basic fibroblast growth factor-2 in combination with beta tricalcium phosphate in class III furcation defects in dogs

Saito

Kuboki

et al. 2013

Dent. Mater. J.

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Section: Discussioncontrasting

confidence: 95%

Periodontal regeneration following application of basic fibroblast growth factor-2 in combination with beta tricalcium phosphate in class III furcation defects in dogs

Saito

Kuboki

et al. 2013

Dent. Mater. J.

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“…It also exhibited a stimulatory action on osteoclasts to resorb bone. All of these findings were similar to those of FGF-2, as shown in our present and previous studies (10,11,13,(15)(16)(17). FGF-10, on the other hand, did not show any regulation on these bone and cartilage cells.…”

Section: Discussionsupporting

confidence: 92%

“…Paradoxically, FGF-2 is also known as a potent stimulator of bone resorption (13)(14)(15)(16)(17) and is involved in joint destruction of rheumatoid arthritis patients (18). The stimulatory effect of FGF-2 on osteoclast formation is mediated by the induction of cyclooxygenase-2, a main regulatory enzyme for prostaglandin production in bone, and receptor activator of nuclear factor-B ligand (RANKL), a key membrane-associated molecule regulating osteoclast differentiation, in osteoblasts (13)(14)(15)17). Other than this indirect action through the mediation of osteoblasts, we recently reported that FGF-2 acts directly on mature osteoclasts to stimulate bone resorption (15,16).…”

mentioning

confidence: 99%

Regulation of Osteoblast, Chondrocyte, and Osteoclast Functions by Fibroblast Growth Factor (FGF)-18 in Comparison with FGF-2 and FGF-10

Shimoaka

Ogasawara

Yonamine

et al. 2002

Journal of Biological Chemistry

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136

101

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This study investigated the actions of fibroblast growth factor (FGF)-18, a novel member of the FGF family, on osteoblasts, chondrocytes, and osteoclasts and compared them with those of FGF-2 and FGF-10. FGF-18 stimulated the proliferation of cultured mouse primary osteoblasts, osteoblastic MC3T3-E1 cells, primary chondrocytes, and prechondrocytic ATDC5 cells, although it inhibited the differentiation and matrix synthesis of these cells. FGF-18 up-regulated the phosphorylation of extracellular signal-regulated kinase in both osteoblasts and chondrocytes and up-regulated the phosphorylation of p38 mitogen-activated protein kinase only in chondrocytes. FGF-18 mitogenic actions were blocked by a specific inhibitor of extracellular signal-regulated kinase in both osteoblasts and chondrocytes and by a specific inhibitor of p38 mitogen-activated protein kinase in chondrocytes. With regard to the action of FGF-18 on bone resorption, FGF-18 not only induced osteoclast formation through receptor activator of nuclear factor-B ligand and cyclooxygenase-2 but also stimulated osteoclast function to form resorbed pits on a dentine slice in the mouse coculture system. All these effects of FGF-18 bore a close resemblance to those of FGF-2, whereas FGF-10 affects none of these cells. FGF-18 may therefore compensate for the action of FGF-2 on bone and cartilage.Fibroblast growth factors (FGFs) 1 are potent mitogens for a wide variety of cells of mesenchymal and neuroectodermal origin (1). FGFs also play a role in the differentiation of a variety of cells and are involved in morphogenesis, angiogenesis, and development. The FGF family now consists of 23 members, FGF-1 to FGF-23, and there are 4 structurally related highaffinity receptors (FGFR1 to FGFR4) belonging to receptor tyrosine kinases that have an intrinsic protein tyrosine kinase activity and elicit tyrosine autophosphorylation of the receptor (1, 2). Recent reports showing that mutations of FGFRs cause several genetic diseases with severe impairment of bone and cartilage formation, such as achondroplasia (3, 4) and thanatophoric dysplasia type II (5), indicate the essential role of FGF signalings on bone and cartilage metabolism.Among FGFs, FGF-2 is well known as a potent regulator of functions of bone and cartilage cells. It is produced by cells of osteoblastic lineage, accumulated in bone matrix, and acts as an autocrine/paracrine factor for bone cells (6 -8). We and others have reported that the exogenous application of FGF-2 has stimulatory effects on bone formation in several in vivo models as a pharmacological action (9 -11). In addition, the Fgf-2-deficient mouse exhibits decreased bone mass and bone formation, although these changes were rather moderate (12). Paradoxically, FGF-2 is also known as a potent stimulator of bone resorption (13-17) and is involved in joint destruction of rheumatoid arthritis patients (18). The stimulatory effect of FGF-2 on osteoclast formation is mediated by the induction of cyclooxygenase-2, a main regulatory enzyme for prostagland...

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“…The inhibition of joint destruction by mPGES-1 deficiency may at least in part be secondary to the inhibition of inflammation of the joints because proinflammatory cytokines, such as tumor necrosis factor ␣, interleukin-1 and -6, and fibroblast growth factor-2, are known to stimulate the differentiation and activation of osteoclasts through the induction of RANKL (for receptor activator of NF-B ligand) in osteoblasts/stromal cells (52)(53)(54)(55). PGE 2 , which is known to be induced by these cytokines, also facilitates RANKL expression (56 -58).…”

Section: Discussionmentioning

confidence: 99%

Reduced Pain Hypersensitivity and Inflammation in Mice Lacking Microsomal Prostaglandin E Synthase-1

Kamei

Yamakawa

Takegoshi

et al. 2004

Journal of Biological Chemistry

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264

245

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We examined the in vivo role of membrane-bound prostaglandin E synthase (mPGES)-1, a terminal enzyme in the PGE 2 -biosynthetic pathway, using mPGES-1 knockout (KO) mice. Comparison of PGES activity in the membrane fraction of tissues from mPGES-1 KO and wild-type (WT) mice indicated that mPGES-1 accounted for the majority of lipopolysaccharide (LPS)-inducible PGES in WT mice. LPS-stimulated production of PGE 2 , but not other PGs, was impaired markedly in mPGES-1-null macrophages, although a low level of cyclooxygenase-2-dependent PGE 2 production still remained. Pain nociception, as assessed by the acetic acid writhing response, was reduced significantly in KO mice relative to WT mice. This phenotype was particularly evident when these mice were primed with LPS, where the stretching behavior and the peritoneal PGE 2 level of KO mice were far less than those of WT mice. Formation of inflammatory granulation tissue and attendant angiogenesis in the dorsum induced by subcutaneous implantation of a cotton thread were reduced significantly in KO mice compared with WT mice. Moreover, collagen antibody-induced arthritis, a model for human rheumatoid arthritis, was milder in KO mice than in WT mice. Collectively, our present results provide unequivocal evidence that mPGES-1 contributes to the formation of PGE 2 involved in pain hypersensitivity and inflammation.

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Regulation of Osteoclast Differentiation by Fibroblast Growth Factor 2: Stimulation of Receptor Activator of Nuclear Factor κB Ligand/Osteoclast Differentiation Factor Expression in Osteoblasts and Inhibition of Macrophage Colony-Stimulating Factor Function in Osteoclast Precursors

Cited by 75 publications

References 38 publications

Periodontal regeneration following application of basic fibroblast growth factor-2 in combination with beta tricalcium phosphate in class III furcation defects in dogs

Periodontal regeneration following application of basic fibroblast growth factor-2 in combination with beta tricalcium phosphate in class III furcation defects in dogs

Regulation of Osteoblast, Chondrocyte, and Osteoclast Functions by Fibroblast Growth Factor (FGF)-18 in Comparison with FGF-2 and FGF-10

Reduced Pain Hypersensitivity and Inflammation in Mice Lacking Microsomal Prostaglandin E Synthase-1

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