FGF2 High Molecular Weight Isoforms Contribute to Osteoarthropathy in Male Mice
Humans with X-linked hypophosphatemia (XLH) and Hyp mice, the murine homolog of the disease, develop severe osteoarthropathy and the precise factors that contribute to this joint degeneration remain largely unknown. Fibroblast growth factor 2 (FGF2) is a key regulatory growth factor in osteoarthriti...
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Published in | Endocrinology (Philadelphia) Vol. 157; no. 12; pp. 4602 - 4614 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Oxford University Press
01.12.2016
Endocrine Society |
Subjects | |
Online Access | Get full text |
ISSN | 0013-7227 1945-7170 1945-7170 |
DOI | 10.1210/en.2016-1548 |
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Abstract | Humans with X-linked hypophosphatemia (XLH) and Hyp mice, the murine homolog of the disease, develop severe osteoarthropathy and the precise factors that contribute to this joint degeneration remain largely unknown. Fibroblast growth factor 2 (FGF2) is a key regulatory growth factor in osteoarthritis. Although there are multiple FGF2 isoforms the potential involvement of specific FGF2 isoforms in joint degradation has not been investigated. Mice that overexpress the high molecular weight FGF2 isoforms in bone (HMWTg mice) phenocopy Hyp mice and XLH subjects and Hyp mice overexpress the HMWFGF2 isoforms in osteoblasts and osteocytes. Given that Hyp mice and XLH subjects develop osteoarthropathies we examined whether HMWTg mice also develop knee joint degeneration at 2, 8, and 18 mo compared with VectorTg (control) mice. HMWTg mice developed spontaneous osteoarthropathy as early as age 2 mo with thinning of subchondral bone, osteophyte formation, decreased articular cartilage thickness, abnormal mineralization within the joint, increased cartilage degradative enzymes, hypertrophic markers, and angiogenesis. FGF receptors 1 and 3 and fibroblast growth factor 23 were significantly altered compared with VectorTg mice. In addition, gene expression of growth factors and cytokines including bone morphogenetic proteins, Insulin like growth factor 1, Interleukin 1 beta, as well as transcription factors Sex determining region Y box 9, hypoxia inducible factor 1, and nuclear factor kappa B subunit 1 were differentially modulated in HMWTg compared with VectorTg. This study demonstrates that overexpression of the HMW isoforms of FGF2 in bone results in catabolic activity in joint cartilage and bone that leads to osteoarthropathy. |
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AbstractList | Humans with X-linked hypophosphatemia (XLH) and Hyp mice, the murine homolog of the disease, develop severe osteoarthropathy and the precise factors that contribute to this joint degeneration remain largely unknown. Fibroblast growth factor 2 (FGF2) is a key regulatory growth factor in osteoarthritis. Although there are multiple FGF2 isoforms the potential involvement of specific FGF2 isoforms in joint degradation has not been investigated. Mice that overexpress the high molecular weight FGF2 isoforms in bone (HMWTg mice) phenocopy Hyp mice and XLH subjects and Hyp mice overexpress the HMWFGF2 isoforms in osteoblasts and osteocytes. Given that Hyp mice and XLH subjects develop osteoarthropathies we examined whether HMWTg mice also develop knee joint degeneration at 2, 8, and 18 mo compared with VectorTg (control) mice. HMWTg mice developed spontaneous osteoarthropathy as early as age 2 mo with thinning of subchondral bone, osteophyte formation, decreased articular cartilage thickness, abnormal mineralization within the joint, increased cartilage degradative enzymes, hypertrophic markers, and angiogenesis. FGF receptors 1 and 3 and fibroblast growth factor 23 were significantly altered compared with VectorTg mice. In addition, gene expression of growth factors and cytokines including bone morphogenetic proteins, Insulin like growth factor 1, Interleukin 1 beta, as well as transcription factors Sex determining region Y box 9, hypoxia inducible factor 1, and nuclear factor kappa B subunit 1 were differentially modulated in HMWTg compared with VectorTg. This study demonstrates that overexpression of the HMW isoforms of FGF2 in bone results in catabolic activity in joint cartilage and bone that leads to osteoarthropathy. Humans with X-linked hypophosphatemia (XLH) and Hyp mice, the murine homolog of the disease, develop severe osteoarthropathy and the precise factors that contribute to this joint degeneration remain largely unknown. Fibroblast growth factor 2 (FGF2) is a key regulatory growth factor in osteoarthritis. Although there are multiple FGF2 isoforms the potential involvement of specific FGF2 isoforms in joint degradation has not been investigated. Mice that overexpress the high molecular weight FGF2 isoforms in bone (HMWTg mice) phenocopy Hyp mice and XLH subjects and Hyp mice overexpress the HMWFGF2 isoforms in osteoblasts and osteocytes. Given that Hyp mice and XLH subjects develop osteoarthropathies we examined whether HMWTg mice also develop knee joint degeneration at 2, 8, and 18 mo compared with VectorTg (control) mice. HMWTg mice developed spontaneous osteoarthropathy as early as age 2 mo with thinning of subchondral bone, osteophyte formation, decreased articular cartilage thickness, abnormal mineralization within the joint, increased cartilage degradative enzymes, hypertrophic markers, and angiogenesis. FGF receptors 1 and 3 and fibroblast growth factor 23 were significantly altered compared with VectorTg mice. In addition, gene expression of growth factors and cytokines including bone morphogenetic proteins, Insulin like growth factor 1, Interleukin 1 beta, as well as transcription factors Sex determining region Y box 9, hypoxia inducible factor 1, and nuclear factor kappa B subunit 1 were differentially modulated in HMWTg compared with VectorTg. This study demonstrates that overexpression of the HMW isoforms of FGF2 in bone results in catabolic activity in joint cartilage and bone that leads to osteoarthropathy.Humans with X-linked hypophosphatemia (XLH) and Hyp mice, the murine homolog of the disease, develop severe osteoarthropathy and the precise factors that contribute to this joint degeneration remain largely unknown. Fibroblast growth factor 2 (FGF2) is a key regulatory growth factor in osteoarthritis. Although there are multiple FGF2 isoforms the potential involvement of specific FGF2 isoforms in joint degradation has not been investigated. Mice that overexpress the high molecular weight FGF2 isoforms in bone (HMWTg mice) phenocopy Hyp mice and XLH subjects and Hyp mice overexpress the HMWFGF2 isoforms in osteoblasts and osteocytes. Given that Hyp mice and XLH subjects develop osteoarthropathies we examined whether HMWTg mice also develop knee joint degeneration at 2, 8, and 18 mo compared with VectorTg (control) mice. HMWTg mice developed spontaneous osteoarthropathy as early as age 2 mo with thinning of subchondral bone, osteophyte formation, decreased articular cartilage thickness, abnormal mineralization within the joint, increased cartilage degradative enzymes, hypertrophic markers, and angiogenesis. FGF receptors 1 and 3 and fibroblast growth factor 23 were significantly altered compared with VectorTg mice. In addition, gene expression of growth factors and cytokines including bone morphogenetic proteins, Insulin like growth factor 1, Interleukin 1 beta, as well as transcription factors Sex determining region Y box 9, hypoxia inducible factor 1, and nuclear factor kappa B subunit 1 were differentially modulated in HMWTg compared with VectorTg. This study demonstrates that overexpression of the HMW isoforms of FGF2 in bone results in catabolic activity in joint cartilage and bone that leads to osteoarthropathy. |
Author | Dealy, Caroline Fisher, Melanie C. Meo Burt, Patience Hurley, Marja M. Xiao, Liping |
Author_xml | – sequence: 1 givenname: Patience surname: Meo Burt fullname: Meo Burt, Patience organization: 1Department of Medicine, Division of Endocrinology and Metabolism, School of Medicine (P.M.B., L.X., M.M.H.), UConn Health, Farmington, CT, 06030-3023 – sequence: 2 givenname: Liping surname: Xiao fullname: Xiao, Liping organization: 1Department of Medicine, Division of Endocrinology and Metabolism, School of Medicine (P.M.B., L.X., M.M.H.), UConn Health, Farmington, CT, 06030-3023 – sequence: 3 givenname: Caroline surname: Dealy fullname: Dealy, Caroline organization: 2Department of Reconstructive Sciences Center for Regenerative Medicine and Skeletal Development, School of Dental Medicine (C.D.), UConn Health, Farmington, CT, 06030-3023 – sequence: 4 givenname: Melanie C. surname: Fisher fullname: Fisher, Melanie C. organization: 1Department of Medicine, Division of Endocrinology and Metabolism, School of Medicine (P.M.B., L.X., M.M.H.), UConn Health, Farmington, CT, 06030-3023 – sequence: 5 givenname: Marja M. surname: Hurley fullname: Hurley, Marja M. email: hurley@uchc.edu organization: 1Department of Medicine, Division of Endocrinology and Metabolism, School of Medicine (P.M.B., L.X., M.M.H.), UConn Health, Farmington, CT, 06030-3023 |
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Snippet | Humans with X-linked hypophosphatemia (XLH) and Hyp mice, the murine homolog of the disease, develop severe osteoarthropathy and the precise factors that... |
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SubjectTerms | Angiogenesis Animals Bone Density - physiology Bone growth Bone morphogenetic proteins Cartilage Cartilage (articular) Cartilage diseases Cartilage, Articular - diagnostic imaging Cartilage, Articular - metabolism Cartilage, Articular - pathology Cytokines - genetics Cytokines - metabolism Degeneration Disease Models, Animal Familial Hypophosphatemic Rickets - diagnostic imaging Familial Hypophosphatemic Rickets - genetics Familial Hypophosphatemic Rickets - metabolism Familial Hypophosphatemic Rickets - pathology Fibroblast growth factor 2 Fibroblast Growth Factor 2 - genetics Fibroblast Growth Factor 2 - metabolism Fibroblast growth factor 23 Fibroblasts Gene Expression Growth factors Hypophosphatemia Hypoxia Intercellular Signaling Peptides and Proteins - genetics Intercellular Signaling Peptides and Proteins - metabolism Interleukin 1 Isoforms Joint diseases Joints (anatomy) Male Mice Mineralization Molecular weight Osteoarthritis Osteocytes Protein Isoforms - genetics Protein Isoforms - metabolism Subchondral bone Transcription factors X-Ray Microtomography |
Title | FGF2 High Molecular Weight Isoforms Contribute to Osteoarthropathy in Male Mice |
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