Structure and Expression of Human Fibroblast Growth Factor-10

Emoto, Hisayo; Tagashira, Shuzo; Matteï, Marie‐Geneviève; Yamasaki, Masahiro; Hashimoto, Gakuji; Katsumata, Takashi; Negoro, Takaharu; Nakatsuka, Masashi; Birnbaum, Daniel; Coulier, François; Itoh, Nobuyuki

doi:10.1074/jbc.272.37.23191

Cited by 113 publications

(78 citation statements)

References 27 publications

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“…Among the 10 gene products well characterized [2][3][4][5], FGF-3 to FGF-8 and FGF-10 are secreted growth factors. FGF-1, FGF-2 and FGF-9 which lack the classical signal peptide, are released from the cell by a mechanism that does not involve the Golgi apparatus.…”

Section: Introductionmentioning

confidence: 99%

Progression in MCF-7 breast cancer cell tumorigenicity: compared effect of FGF-3 and FGF-4

Hajitou

Deroanne

Noël

et al. 2000

Breast Cancer Res Treat

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SummaryThe transforming properties of fibroblast growth factor 3 (FGF-3) were investigated in MCF7 breast cancer cells and compared to those of FGF-4, a known oncogenic product. The short form of fgf-3 and the fgf-4 sequences were each introduced with retroviral vectors and the proteins were only detected in the cytoplasm of the infected cells, as expected. In vitro, cells producing FGF-3 (MCF7.fgf-3) and FGF-4 (MCF7.fgf-4) displayed an amount of estrogen receptors decreased to around 45% of the control value. However, MCF7.fgf-3 cell proliferation remained responsive to estradiol supply. The sensitivity of the MCF7.fgf-4 cells, if existant, was masked by the important mitogenic action exerted by FGF-4. In vivo, the MCF7.fgf-3 and MCF7.fgf-4 cells gave rise to tumors under conditions in which the control cells were not tumorigenic. Supplementing the mice with estrogen had the paradoxical effect of totally suppressing the start of the FGF-3 as well as the FGF-4 tumors. Tumorigenicity in the presence of matrigel was similar for MCF7.fgf-3 and control cells and was increased by estrogen supplementation. Once started, the MCF7.fgf-4 tumors grew with a characteristic high rate. Remarkably, FGF-4 but not FGF-3, stimulated the secretion of vascular endothelial growth factor (VEGF 165 ) without altering the steady-state level of its mRNA, suggesting a possible regulation of VEGF synthesis at the translational level in MCF7 cells. The increased VEGF secretion is probably involved in the more aggressive phenotype of the MCF7.fgf-4 cells while a decreased dependence upon micro-environmental factors might be part of the increased tumorigenic potential of the MCF7.fgf-3 cells.

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Section: Introductionmentioning

confidence: 99%

Progression in MCF-7 breast cancer cell tumorigenicity: compared effect of FGF-3 and FGF-4

Hajitou

Deroanne

Noël

et al. 2000

Breast Cancer Res Treat

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“…The antibodies to FGF10 used for immunoblot analysis were produced by immunization of hens with recombinant human FGF10 (Emoto et al 1997). The antibodies to PPAR␥ (Hu et al 1996) and adipsin (Cook et al 1987) were kindly provided by B.M.…”

Section: Antibodiesmentioning

confidence: 99%

Requirement of fibroblast growth factor 10 in development of white adipose tissue

Sakaue¹,

Konishi²,

Ogawa³

et al. 2002

Genes Dev.

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118

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Fibroblast growth factors (FGFs) are important intercellular signaling molecules in developmental processes.Here, we show that FGF10 is secreted by cultured preadipocytes and that prevention of FGF10 signaling inhibits the expression of C/EBP␤ and the subsequent differentiation of these cells. An active form of C/EBP␤ rescued differentiation of the cells in which FGF10 signaling was blocked. Development of white adipose tissue and the expression of C/EBP␤ in this tissue of FGF10 knockout mice were markedly reduced, and the ability of embryonic fibroblasts derived from FGF10 knockout mice to differentiate into adipocytes was impaired. Therefore, FGF10 plays an important role in adipogenesis, at least partly by contributing to the expression of C/EBP␤ through an autocrine/paracrine mechanism. Received February 8, 2002; revised version accepted March 1, 2002. Adipose tissue contributes to regulation of energy balance, not only by serving as a reservoir of triglycerides but also by secreting circulating factors that affect food intake or metabolism (Hwang et al. 1997;Rosen and Spiegelman 2000;Fruebis et al. 2001;Steppan et al. 2001). Mature adipocytes do not undergo cell division; the number of these cells is therefore thought to increase as a result of the proliferation of preadipocytes and their subsequent differentiation into mature adipocytes. Various factors secreted by adipocytes or preadipocytes have been identified (Hwang et al. 1997;Rosen and Spiegelman 2000;MacDougald and Mandrup 2002), some of which, such as tumor necrosis factor-␣ (Petrunschke and Hauner 1994), Pref-1 (Smas et al. 1997), and Wnt-10b (Ross et al. 2000), regulate adipogenesis by inhibiting the differentiation of these cells. Although factors that promote the proliferation or differentiation of preadipocytes have also been shown to be secreted by such cells isolated from obese humans (Lau et al. 1987) or by mature rat adipocytes (Schillabeer et al. 1989), the nature of these factors has remained unclear.The fibroblast growth factor (FGF) family comprises at least 23 proteins (Yamashita et al. 2000;Ornitz and Itoh 2001) that function in an autocrine or paracrine manner and play important roles in the development, maintenance, and repair of tissues (Goldfarb 1996;Ornitz and Itoh 2001). FGF10 was initially identified in rat embryos by homology-based polymerase chain reaction (PCR; Yamasaki et al. 1996). Disruption of the FGF10 gene resulted in complete absence of limb bud formation and severe defects in the branching morphogenesis of the lung (Min et al. 1998;Sekine et al. 1999), indicating that FGF10 is important for development of these organs. On the other hand, we have previously shown that, among the major adult tissues, transcripts of the FGF10 gene are most abundant in adipose tissue . Brown adipose tissue (BAT) and white adipose tissue (WAT) constitute the two principal types of adipose tissue and perform distinct functions (Hwang et al. 1997;Rosen and Spiegelman 2000). The expression of FGF10 is restricted to WAT. In particular, F...

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“…KGF-2 is mainly expressed and secreted by stromal cells and has a high affinity to fibroblast growth factor receptor 2-IIIb, which is mainly expressed on the epithelium; it has a comparatively weaker affinity for fibroblast growth factor receptor 1-IIIb expressed by epithelial and endothelial cells [4][5][6][7]. KGF-2 has been found to play an essential role in epithelial-mesenchymal interactions for the proper development of organs such as the lungs [5].…”

Section: Introductionmentioning

confidence: 99%

KGF-2 ameliorates acute lung injury via inhibiting TH17 cells-NF-κB-dependent inflammation and activating the PI3K/Akt survival signaling pathway in mice

Wang¹,

Wang²,

Ji³

et al. 2018

Oncotarget

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Acute lung injury is characterized by alveolar injury, inflammation, and infiltration of inflammatory cells. Although the protective effects of keratinocyte growth factor-2 on ALI have been defined, the mechanisms remain unclear. Lipopolysaccharides (Pseudomonas aeruginosa) was administered intratracheally into mice lungs, and peak lung injury occurred on day 6 after the LPS challenge, with resolution on day 10. A progressive influx of CD4 + CD25 + Foxp3 + T cells into the lungs and spleen on day 1, which peaked on day 6, and was maintained at high level on day 10. The percentage of Th17 cells in lung tissue and blood was higher in the ALI group than in the control group, which peaked on day 2, and returned to nearly normal on day 10. KGF-2 attenuated lung injury by inhibiting the prevalence of Th17 cells through STAT3 dysfunction and NF-κB signal, and improved survival rate by activating the PI3K/Akt signal. These results illustrated a new mechanism of KGF-2 on ALI by inhibiting Th17 cells mediated by STAT3-NF-κB, and activating the PI3k/Akt signal.

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Structure and Expression of Human Fibroblast Growth Factor-10

Cited by 113 publications

References 27 publications

Progression in MCF-7 breast cancer cell tumorigenicity: compared effect of FGF-3 and FGF-4

Progression in MCF-7 breast cancer cell tumorigenicity: compared effect of FGF-3 and FGF-4

Requirement of fibroblast growth factor 10 in development of white adipose tissue

KGF-2 ameliorates acute lung injury via inhibiting TH17 cells-NF-κB-dependent inflammation and activating the PI3K/Akt survival signaling pathway in mice

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