Research Progress of Fibroblast Growth Factor 8’s Role in the Regulation of Bone Development and Homeostasis

HUANG Hong-can, WEI Jie-ya, ZHANG De-mao, ZHOU Xue-dong

Abstract

The proper development and the homeostasis maintenance of bones are important prerequisites for the normal functioning of the human body. Bone developmental deformities or homeostasis disorders, such as Kashin-Beck disease, craniosynostosis, cleft palate and osteoarthritis, severely affect the life of patients, causing significant stress to the family and the society. Fibroblast growth factor 8 (FGF8) plays multiple functions through the course of the life of organisms. Abnormal expression of FGF8 may cause disorders of bone homeostasis and developmental abnormalities of bones. More and more studies have found that FGF8 may play an important role in bone development and may become a potential therapeutic target. Herein, we reviewed the role of FGF8 in a variety of skeletal abnormalities, intending to provide new perspectives for the prevention and treatment of related diseases in the future.

 

Keywords: Fibroblast growth factor 8, Craniosynostosis, Cleft palate, Osteoarthritis, Kashin-Beck disease

 

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References


ORNITZ D M, ITOH N. The fibroblast growth factor signaling pathway. Wiley Interdiscip Rev Dev Biol,2015,4(3): 215–266.

ARMELIN H A. Pituitary extracts and steroid hormones in the control of 3T3 cell growth. Proc Natl Acad Sci U S A,1973,70(9): 2702–2706. ITOH N, ORNITZ D M. Evolution of the FGF and FGFR gene families. Trends Genet,2004,20(11): 563–569.

TANAKA A, MIYAMOTO K, MINAMINO N, et al. Cloning and characterization of an androgen-induced growth factor essential for the androgen-dependent growth of mouse mammary carcinoma cells. Proc Natl Acad Sci U S A,1992,89(19): 8928–8932.

GOETZ R, MOHAMMADI M. Exploring mechanisms of FGF signalling through the lens of structural biology. Nat Rev Mol Cell Biol,2013,14(3): 166–180.

ZHANG X, IBRAHIMI O A, OLSEN S K, et al. Receptor specificity of the fibroblast growth factor family. The complete mammalian FGF family. J Biol Chem,2006,281(23): 15694–15700.

MEYERS E N, LEWANDOSKI M, MARTIN G R. An FGF8 mutant allelic series generated by Cre- and Flp-mediated recombination. Nat Genet,1998,18(2): 136–141.

NAICHE L A, HOLDER N, LEWANDOSKI M. FGF4 and FGF8 comprise the wavefront activity that controls somitogenesis. Proc Natl Acad Sci U S A,2011,108(10): 4018–4023.

PARK E J, OGDEN L A, TALBOT A, et al. Required, tissue-specific roles for FGF8 in outflow tract formation and remodeling. Development, 2006,133(12): 2419–2433.

HASEGAWA K, SAGA Y. FGF8-FGFR1 signaling acts as a niche factor for maintaining undifferentiated spermatogonia in the mouse. Biol Reprod, 2014, 91(6): 145[2021-09-15]. https://doi.org/10.1095/biolreprod.114.121012.

ORNITZ D M, MARIE P J. Fibroblast growth factor signaling in skeletal development and disease. Genes Dev,2015,29(14): 1463–1486.

LIN J M, CALLON K E, LIN J S, et al. Actions of fibroblast growth factor-8 in bone cells in vitro. Am J Physiol Endocrinol Metab,2009, 297(1): E142–150.

LEWANDOSKI M, SUN X, MARTIN G R. FGF8 signalling from the AER is essential for normal limb development. Nat Genet,2000,26(4): 460–463.

TRUMPP A, DEPEW M J, RUBENSTEIN J L, et al. Cre-mediated gene inactivation demonstrates that FGF8 is required for cell survival and patterning of the first branchial arch. Genes Dev,1999,13(23): 3136–3148.

ELLMAN M B, YAN D, AHMADINIA K, et al. Fibroblast growth factor control of cartilage homeostasis. J Cell Biochem,2013,114(4): 735–742.

GLYN-JONES S, PALMER A J, AGRICOLA R, et al. Osteoarthritis. Lancet,2015,386(9991): 376–387.

ZHANG Z, HUANG C, JIANG Q, et al. Guidelines for the diagnosis and treatment of osteoarthritis in China (2019 edition). Ann Transl Med, 2020, 8(19): 1213[2021-09-15]. https://doi.org/10.21037/atm-20-4665.

MARTEL-PELLETIER J, BARR A J, CICUTTINI F M, et al. Osteoarthritis. Nat Rev Dis Primers, 2016, 2: 16072[2021-9-15]. https://www.nature.com/articles/nrdp201672. doi: 10.1038/nrdp.2016.72.

KIM J W, CHUNG M K, LEE J, et al. Association of periodontitis with radiographic knee osteoarthritis. J Periodontol,2020,91(3): 369–376.

CROSS M, SMITH E, HOY D, et al. The global burden of hip and knee osteoarthritis: Estimates from the global burden of disease 2010 study. Ann Rheum Dis,2014,73(7): 1323–1330.

TANG X, WANG S, ZHAN S, et al. The prevalence of symptomatic knee osteoarthritis in china: Results from the China Health and Retirement Longitudinal Study. Arthritis Rheumatol,2016,68(3): 648–653.

UCHII M, TAMURA T, SUDA T, et al. Role of fibroblast growth factor 8 (FGF8) in animal models of osteoarthritis. Arthritis Res Ther, 2008, 10(4): R90[2021-09-15]. https://doi.org/10.1186/ar2474.

WAN J, ZHANG G, LI X, et al. Matrix metalloproteinase 3: A promoting and destabilizing factor in the pathogenesis of disease and cell differentiation. Front Physiol, 2021, 12: 663978[2021-09-15]. https://doi.org/10.3389/fphys.2021.663978.

HARDY M M, SEIBERT K, MANNING P T, et al. Cyclooxygenase 2-dependent prostaglandin E2 modulates cartilage proteoglycan degradation in human osteoarthritis explants. Arthritis Rheum,2002, 46(7): 1789–1803.

BURRAGE P S , MIX K S, BRINCKERHOFF C E. Matrix metalloproteinases: role in arthritis. Front Biosci,2006,11: 529–543.

XIE J, WANG C L, YANG W, et al. Modulation of MMP-2 and MMP-9 through connected pathways and growth factors is critical for extracellular matrix balance of intra-articular ligaments. J Tissue Eng Regen Med, 2018, 12(1): e550-e565[2021-09-15]. https://doi.org/10.1002/term.2325.

STONE R. Diseases. A medical mystery in middle China. Science,2009, 324(5933): 1378–1381.

GUO X, MA W J, ZHANG F, et al. Recent advances in the research of an endemic osteochondropathy in China: Kashin-Beck disease. Osteoarthritis Cartilage,2014,22(11): 1774–1783.

LIU H, FANG Q, WANG M, et al. FGF8 and FGFR3 are up-regulated in hypertrophic chondrocytes: Association with chondrocyte death in deep zone of Kashin-Beck disease. Biochem Biophys Res Commun,2018, 500(2): 184–190.


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