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El-Seoudi A, Abd El Kader T, Nishida T, et al. Catabolic effects of FGF-1 on chondrocytes and its possible role in osteoarthritis. J Cell Commun Signal. 2017;11(3):255-263doi: 10.1007/s12079-017-0384-8.
El-Seoudi, A., Abd El Kader, T., Nishida, T., Eguchi, T., Aoyama, E., Takigawa, M., & Kubota, S. (2017). Catabolic effects of FGF-1 on chondrocytes and its possible role in osteoarthritis. Journal of cell communication and signaling, 11(3), 255-263. https://doi.org/10.1007/s12079-017-0384-8
El-Seoudi, Abdellatif, et al. "Catabolic effects of FGF-1 on chondrocytes and its possible role in osteoarthritis." Journal of cell communication and signaling vol. 11,3 (2017): 255-263. doi: https://doi.org/10.1007/s12079-017-0384-8
El-Seoudi A, Abd El Kader T, Nishida T, Eguchi T, Aoyama E, Takigawa M, Kubota S. Catabolic effects of FGF-1 on chondrocytes and its possible role in osteoarthritis. J Cell Commun Signal. 2017 Sep;11(3):255-263. doi: 10.1007/s12079-017-0384-8. Epub 2017 Mar 25. PMID: 28343287; PMCID: PMC5559396.
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J Cell Commun Signal. 2017 Sep;11(3):255-263. doi: 10.1007/s12079-017-0384-8. Epub 2017 Mar 25.

Catabolic effects of FGF-1 on chondrocytes and its possible role in osteoarthritis.

Journal of cell communication and signaling

Abdellatif El-Seoudi, Tarek Abd El Kader, Takashi Nishida, Takanori Eguchi, Eriko Aoyama, Masaharu Takigawa, Satoshi Kubota

Affiliations

  1. Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Kita-ku, Okayama, 700-8525, Japan.
  2. Advanced Research Center for Oral and Craniofacial Sciences, Okayama University Dental School, Okayama, Japan.
  3. Department of Dental Pharmacology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
  4. Advanced Research Center for Oral and Craniofacial Sciences, Okayama University Dental School, Okayama, Japan. [email protected].
  5. Department of Biochemistry and Molecular Dentistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Kita-ku, Okayama, 700-8525, Japan. [email protected].
  6. Advanced Research Center for Oral and Craniofacial Sciences, Okayama University Dental School, Okayama, Japan. [email protected].

PMID: 28343287 PMCID: PMC5559396 DOI: 10.1007/s12079-017-0384-8

Abstract

Fibroblast growth factor 1 (FGF-1) is a classical member of the FGF family and is produced by chondrocytes cultured from osteoarthritic patients. Also, this growth factor was shown to bind to CCN family protein 2 (CCN2), which regenerates damaged articular cartilage and counteracts osteoarthritis (OA) in an animal model. However, the pathophysiological role of FGF-1 in cartilage has not been well investigated. In this study, we evaluated the effects of FGF-1 in vitro and its production in vivo by use of an OA model. Treatment of human chondrocytic cells with FGF-1 resulted in marked repression of genes for cartilaginous extracellular matrix components, whereas it strongly induced matrix metalloproteinase 13 (MMP-13), representing its catabolic effects on cartilage. Interestingly, expression of the CCN2 gene was dramatically repressed by FGF-1, which repression eventually caused the reduced production of CCN2 protein from the chondrocytic cells. The results of a reporter gene assay revealed that this repression could be ascribed, at least in part, to transcriptional regulation. In contrast, the gene expression of FGF-1 was enhanced by exogenous FGF-1, indicating a positive feedback system in these cells. Of note, induction of FGF-1 was observed in the articular cartilage of a rat OA model. These results collectively indicate a pathological role of FGF-1 in OA development, which includes an insufficient cartilage regeneration response caused by CCN2 down regulation.

Keywords: CCN2; Cartilage; Chondrocytes; FGF-1; Osteoarthritis

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