دورية أكاديمية
Syndecan-3 enhances anabolic bone formation through WNT signaling.
العنوان: | Syndecan-3 enhances anabolic bone formation through WNT signaling. |
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المؤلفون: | Johnson de Sousa Brito FM; Department of Musculoskeletal and Ageing Science (formerly Department of Musculoskeletal Biology), Institute of Life Course and Medical Sciences (formerly Institute of Ageing and Chronic Disease), University of Liverpool, Liverpool, UK., Butcher A; Department of Musculoskeletal and Ageing Science (formerly Department of Musculoskeletal Biology), Institute of Life Course and Medical Sciences (formerly Institute of Ageing and Chronic Disease), University of Liverpool, Liverpool, UK., Pisconti A; Department of Biochemistry, IIB, University of Liverpool, Liverpool, UK.; Department of Biochemistry and Cell Biology, Stony Brook University, Stony Brook, NY, USA., Poulet B; Department of Musculoskeletal and Ageing Science (formerly Department of Musculoskeletal Biology), Institute of Life Course and Medical Sciences (formerly Institute of Ageing and Chronic Disease), University of Liverpool, Liverpool, UK., Prior A; Department of Musculoskeletal and Ageing Science (formerly Department of Musculoskeletal Biology), Institute of Life Course and Medical Sciences (formerly Institute of Ageing and Chronic Disease), University of Liverpool, Liverpool, UK., Charlesworth G; Department of Musculoskeletal and Ageing Science (formerly Department of Musculoskeletal Biology), Institute of Life Course and Medical Sciences (formerly Institute of Ageing and Chronic Disease), University of Liverpool, Liverpool, UK., Sperinck C; Department of Musculoskeletal and Ageing Science (formerly Department of Musculoskeletal Biology), Institute of Life Course and Medical Sciences (formerly Institute of Ageing and Chronic Disease), University of Liverpool, Liverpool, UK., Scotto di Mase M; Department of Musculoskeletal and Ageing Science (formerly Department of Musculoskeletal Biology), Institute of Life Course and Medical Sciences (formerly Institute of Ageing and Chronic Disease), University of Liverpool, Liverpool, UK., Liu K; Department of Musculoskeletal and Ageing Science (formerly Department of Musculoskeletal Biology), Institute of Life Course and Medical Sciences (formerly Institute of Ageing and Chronic Disease), University of Liverpool, Liverpool, UK., Bou-Gharios G; Department of Musculoskeletal and Ageing Science (formerly Department of Musculoskeletal Biology), Institute of Life Course and Medical Sciences (formerly Institute of Ageing and Chronic Disease), University of Liverpool, Liverpool, UK., Jurgen van 't Hof R; Department of Musculoskeletal and Ageing Science (formerly Department of Musculoskeletal Biology), Institute of Life Course and Medical Sciences (formerly Institute of Ageing and Chronic Disease), University of Liverpool, Liverpool, UK., Daroszewska A; Department of Musculoskeletal and Ageing Science (formerly Department of Musculoskeletal Biology), Institute of Life Course and Medical Sciences (formerly Institute of Ageing and Chronic Disease), University of Liverpool, Liverpool, UK.; Department of Clinical Biochemistry and Metabolic Medicine, Liverpool University Hospitals NHS Foundation Trust, Liverpool, UK.; Department of Rheumatology, Liverpool University Hospitals NHS Foundation Trust, Liverpool, UK. |
المصدر: | FASEB journal : official publication of the Federation of American Societies for Experimental Biology [FASEB J] 2021 Apr; Vol. 35 (4), pp. e21246. |
نوع المنشور: | Journal Article; Research Support, Non-U.S. Gov't |
اللغة: | English |
بيانات الدورية: | Publisher: Federation of American Societies for Experimental Biology Country of Publication: United States NLM ID: 8804484 Publication Model: Print Cited Medium: Internet ISSN: 1530-6860 (Electronic) Linking ISSN: 08926638 NLM ISO Abbreviation: FASEB J Subsets: MEDLINE |
أسماء مطبوعة: | Publication: 2020- : [Bethesda, Md.] : Hoboken, NJ : Federation of American Societies for Experimental Biology ; Wiley Original Publication: [Bethesda, Md.] : The Federation, [c1987- |
مواضيع طبية MeSH: | Bone Development/*physiology , Syndecan-3/*metabolism , Wnt Signaling Pathway/*physiology, Animals ; Animals, Newborn ; Antibodies ; Cell Proliferation ; Fetal Development ; Male ; Mice ; Mice, Knockout ; Osteoblasts ; Osteoclasts ; Syndecan-3/genetics |
مستخلص: | Osteoporosis is the most common age-related metabolic bone disorder, which is characterized by low bone mass and deterioration in bone architecture, with a propensity to fragility fractures. The best treatment for osteoporosis relies on stimulation of osteoblasts to form new bone and restore bone structure, however, anabolic therapeutics are few and their use is time restricted. Here, we report that Syndecan-3 increases new bone formation through enhancement of WNT signaling in osteoblasts. Young adult Sdc3 -/- mice have low bone volume, reduced bone formation, increased bone marrow adipose tissue, increased bone fragility, and a blunted anabolic bone formation response to mechanical loading. This premature osteoporosis-like phenotype of Sdc3 -/- mice is due to delayed osteoblast maturation and impaired osteoblast function, with contributing increased osteoclast-mediated bone resorption. Indeed, overexpressing Sdc3 in osteoblasts using the Col1a1 promoter rescues the low bone volume phenotype of the Sdc3 -/- mice, and also increases bone volume in WT mice. Mechanistically, SDC3 enhances canonical WNT signaling in osteoblasts through stabilization of Frizzled 1, making SDC3 an attractive target for novel bone anabolic drug development. (© 2020 The Authors. The FASEB Journal published by Wiley Periodicals LLC on behalf of Federation of American Societies for Experimental Biology.) |
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معلومات مُعتمدة: | MR/P020941/1 United Kingdom MRC_ Medical Research Council; MR/R002819/1 RCUK | Medical Research Council (MRC) |
فهرسة مساهمة: | Keywords: Syndecan-3; WNT; bone; frizzled; osteoblast |
المشرفين على المادة: | 0 (Antibodies) 0 (Sdc3 protein, mouse) 0 (Syndecan-3) |
تواريخ الأحداث: | Date Created: 20210326 Date Completed: 20210719 Latest Revision: 20220216 |
رمز التحديث: | 20221213 |
مُعرف محوري في PubMed: | PMC8251628 |
DOI: | 10.1096/fj.202002024R |
PMID: | 33769615 |
قاعدة البيانات: | MEDLINE |
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