Fibroblast growth factor-18 is a trophic factor for mature chondrocytes and their progenitors

Ellsworth, Jeff L.; Berry, J. L.; Bukowski, Thomas R.; Claus, Juan Daniel; Feldhaus, Andrew L.; Holderman, Susan; Holdren, Matthew S.; Lum, Karen D.; Moore, Emma; Raymond, F. Lucy; Ren, Hong-Ping; Shea, Patrick R.; Sprecher, Cindy A.; Storey, H. H.; Thompson, Deborah; Waggie, Kim; Yao, Lena; Fernandes, Russell J.; Eyre, David R.; Hughes, Steven D.

doi:10.1053/joca.2002.0514

Cited by 180 publications

(166 citation statements)

References 31 publications

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“…Specifically, FGFR1 and FGFR3 were most highly expressed in human articular chondrocytes. These results were similar to those reported by Ellsworth et al, who demonstrated the basal expression of FGFR2 and FGFR3 in normal adult articular chondrocytes; however, their findings did not include the study of FGFR1 (Ellsworth et al, 2002).…”

Section: (C) Extracellular Signaling Mediated By Bfgfsupporting

confidence: 91%

“…In contrast to the controversial role of bFGF in articular and IVD cartilage, FGF-18 has been shown to have significant anabolic effects on chondrocytes in a variety of cartilaginous tissues (Ellsworth et al, 2002;Ohbayashi et al, 2002). Local delivery of adenovirus expressing Fgf18 into the pinnae of nude mice increased the formation of auricular cartilage, type II collagen formation, PG production, and chondrocyte proliferation (Ellsworth et al, 2002).…”

Section: Fgf-18 (A) Fgf-18 In Articular Cartilagementioning

confidence: 99%

“…Local delivery of adenovirus expressing Fgf18 into the pinnae of nude mice increased the formation of auricular cartilage, type II collagen formation, PG production, and chondrocyte proliferation (Ellsworth et al, 2002). Systemic delivery of pharmacologic doses of FGF-18 to rats via a single intravenous injection stimulated expansion of various cartilage depots, including the rib-sternum junction, trachea, spine, and articular cartilage within a 2-week period (Ellsworth et al, 2002).…”

Section: Fgf-18 (A) Fgf-18 In Articular Cartilagementioning

confidence: 99%

“…In mature cartilage, FGF-18 has been shown to stimulate cell proliferation, ECM production, and PG synthesis in primary porcine and human adult articular chondrocytes (Ellsworth et al, 2002) and the growth of neonatal rat costal chondrocytes (Shimoaka et al, 2002). Further, Moore et al were the first to study the potential for in vivo cartilage repair by FGF-18 via intra-articular injection in a rat meniscal tear model of OA (Moore et al, 2005).…”

Section: Fgf-18 (A) Fgf-18 In Articular Cartilagementioning

confidence: 99%

“…In contrast to the controversial role of bFGF in joint and spine disc cartilage, FGF-18 is a well-known anabolic growth factor involved in osteogenesis, chondrogenesis, and articular cartilage repair (Ellsworth et al, 2002;Liu et al, 2002;Ohbayashi et al, 2002;Davidson et al, 2005;Moore et al, 2005), and here we will review its role in joint cartilage. To date, the role of FGF-18 in the IVD has yet to be studied.…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

Biological impact of the fibroblast growth factor family on articular cartilage and intervertebral disc homeostasis

Ellman

Muddasani

et al. 2008

Gene

152

131

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Section: (C) Extracellular Signaling Mediated By Bfgfsupporting

confidence: 91%

Section: Fgf-18 (A) Fgf-18 In Articular Cartilagementioning

confidence: 99%

Section: Fgf-18 (A) Fgf-18 In Articular Cartilagementioning

confidence: 99%

Section: Fgf-18 (A) Fgf-18 In Articular Cartilagementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Biological impact of the fibroblast growth factor family on articular cartilage and intervertebral disc homeostasis

Ellman

Muddasani

et al. 2008

Gene

152

131

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Sympathetic Neurotransmitter, VIP, Delays Intervertebral Disc Degeneration via FGF18/FGFR2‐Mediated Activation of Akt Signaling Pathway

Sun,

Yan

et al. 2023

Advanced Biology

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Neuromodulation‐related intervertebral disc degeneration (IVDD) is a novel IVDD pattern and are proposed recently. However, the mechanistic basis of neuromodulation and intervertebral disc (IVD) homeostasis remains unclear. Here, this study aimed to investigate the expression of postganglionic sympathetic nerve fiber‐derived vasoactive intestinal peptide (VIP) system in human IVD tissue, and to assess the role of VIP‐related neuromodulation in IVDD. Patient samples and in vitro cell experiments showed that the expression of receptors for VIP is negatively correlated with the severity of IVDD, and the administration of exogenous VIP can ameliorate interleukin 1β‐induced nucleus pulposus (NP) cell apoptosis and inflammation. Further mRNA‐seq analysis revealed that fibroblast growth factor 18‐ (FGF18)‐mediated activation of V‐akt murine thymoma viral oncogene homolog signaling pathway is involved in the protective effects of VIP on inflammation‐induced NP cell degeneration. Further analysis identified VIP via its receptor vasoactive intestinal peptide receptor 2 can directly result in decreased expression of miR‐15a‐5p, which targeted FGF18. Finally, in vivo mice lumbar IVDD model confirmed that focally exogenous administration of VIP can effectively ameliorated the progression of IVDD, as shown by the radiological and histological analysis. In conclusion, these results indicated that sympathetic neurotransmitter, VIP, delayed IVDD via FGF18/FGFR2‐mediated activation of V‐akt murine thymoma viral oncogene homolog signaling pathway, which will broaden the horizon concerning how the neuromodulation correlates with IVDD and shed new light on novel therapeutical alternatives to IVDD.

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Sulfated Hydrogel Matrices Direct Mitogenicity and Maintenance of Chondrocyte Phenotype through Activation of FGF Signaling

Öztürk

Arlov

Aksel

et al. 2016

Adv Funct Materials

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Deciphering the roles of chemical and physical features of the extracellular matrix (ECM) is vital for developing biomimetic materials with desired cellular responses in regenerative medicine. Here, we demonstrate that sulfation of biopolymers, mimicking the proteoglycans in native tissues, induces mitogenicity, chondrogenic phenotype, and suppresses catabolic activity of chondrocytes, a cell type that resides in a highly sulfated tissue. We show through tunable modification of alginate that increased sulfation of the microenvironment promotes FGF signaling-mediated proliferation of chondrocytes in a three-dimensional (3D) matrix independent of stiffness, swelling, and porosity. Furthermore, we show for the first time that a biomimetic hydrogel acts as a 3D signaling matrix to mediate a heparan sulfate/heparin-like interaction between FGF and its receptor leading to signaling cascades inducing cell proliferation, cartilage matrix production, and suppression of de-differentiation markers. Collectively, this study reveals important insights on mimicking the ECM to guide self-renewal of cells via manipulation of distinct signaling mechanisms.

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Fibroblast growth factor-18 is a trophic factor for mature chondrocytes and their progenitors

Cited by 180 publications

References 31 publications

Biological impact of the fibroblast growth factor family on articular cartilage and intervertebral disc homeostasis

Biological impact of the fibroblast growth factor family on articular cartilage and intervertebral disc homeostasis

Sympathetic Neurotransmitter, VIP, Delays Intervertebral Disc Degeneration via FGF18/FGFR2‐Mediated Activation of Akt Signaling Pathway

Sulfated Hydrogel Matrices Direct Mitogenicity and Maintenance of Chondrocyte Phenotype through Activation of FGF Signaling

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