دورية أكاديمية
أعرض في EDS

Nuclear Factor-Kappa B Regulation of Osteoclastogenesis and Osteoblastogenesis.

التفاصيل البيبلوغرافية
العنوان: Nuclear Factor-Kappa B Regulation of Osteoclastogenesis and Osteoblastogenesis.
المؤلفون: Boyce BF; Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY, USA.; Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, NY, USA., Li J; Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY, USA.; Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, NY, USA., Yao Z; Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY, USA.; Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, NY, USA., Xing L; Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, Rochester, NY, USA.; Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, NY, USA.
المصدر: Endocrinology and metabolism (Seoul, Korea) [Endocrinol Metab (Seoul)] 2023 Oct; Vol. 38 (5), pp. 504-521. Date of Electronic Publication: 2023 Sep 26.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural
اللغة: English
بيانات الدورية: Publisher: Korean Endocrine Society Country of Publication: Korea (South) NLM ID: 101554139 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 2093-5978 (Electronic) Linking ISSN: 2093596X NLM ISO Abbreviation: Endocrinol Metab (Seoul) Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Seoul : Korean Endocrine Society, [2010]-
مواضيع طبية MeSH: NF-kappa B*/metabolism , Osteogenesis*, Mice ; Animals ; TNF Receptor-Associated Factor 3/metabolism ; Ligands ; Osteoclasts/metabolism ; Osteoclasts/pathology ; Transforming Growth Factor beta/metabolism
مستخلص: Maintenance of skeletal integrity requires the coordinated activity of multinucleated bone-resorbing osteoclasts and bone-forming osteoblasts. Osteoclasts form resorption lacunae on bone surfaces in response to cytokines by fusion of precursor cells. Osteoblasts are derived from mesenchymal precursors and lay down new bone in resorption lacunae during bone remodeling. Nuclear factorkappa B (NF-κB) signaling regulates osteoclast and osteoblast formation and is activated in osteoclast precursors in response to the essential osteoclastogenic cytokine, receptor activator of NF-κB ligand (RANKL), which can also control osteoblast formation through RANK-RANKL reverse signaling in osteoblast precursors. RANKL and some pro-inflammatory cytokines, including tumor necrosis factor (TNF), activate NF-κB signaling to positively regulate osteoclast formation and functions. However, these cytokines also limit osteoclast and osteoblast formation through NF-κB signaling molecules, including TNF receptor-associated factors (TRAFs). TRAF6 mediates RANKL-induced osteoclast formation through canonical NF-κB signaling. In contrast, TRAF3 limits RANKL- and TNF-induced osteoclast formation, and it restricts transforming growth factor β (TGFβ)-induced inhibition of osteoblast formation in young and adult mice. During aging, neutrophils expressing TGFβ and C-C chemokine receptor type 5 (CCR5) increase in bone marrow of mice in response to increased NF-κB-induced CC motif chemokine ligand 5 (CCL5) expression by mesenchymal progenitor cells and injection of these neutrophils into young mice decreased bone mass. TGFβ causes degradation of TRAF3, resulting in decreased glycogen synthase kinase-3β/β-catenin-mediated osteoblast formation and age-related osteoporosis in mice. The CCR5 inhibitor, maraviroc, prevented accumulation of TGFβ+/CCR5+ neutrophils in bone marrow and increased bone mass by inhibiting bone resorption and increasing bone formation in aged mice. This paper updates current understanding of how NF-κB signaling is involved in the positive and negative regulation of cytokine-mediated osteoclast and osteoblast formation and activation with a focus on the role of TRAF3 signaling, which can be targeted therapeutically to enhance bone mass.
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معلومات مُعتمدة: R01 AR063650 United States AR NIAMS NIH HHS; R01 AG076731 United States AG NIA NIH HHS; R01 AG049994 United States AG NIA NIH HHS; R01 AR043510 United States AR NIAMS NIH HHS
فهرسة مساهمة: Keywords: Aging; Osteoblasts; Osteoclasts; Osteoporosis; TNF receptor-associated factor 3; TNF receptor-associated factor 6; Transforming growth factor-beta
المشرفين على المادة: 0 (NF-kappa B)
0 (TNF Receptor-Associated Factor 3)
0 (Ligands)
0 (Transforming Growth Factor beta)
تواريخ الأحداث: Date Created: 20230926 Date Completed: 20231030 Latest Revision: 20231107
رمز التحديث: 20231107
مُعرف محوري في PubMed: PMC10613774
DOI: 10.3803/EnM.2023.501
PMID: 37749800
قاعدة البيانات: MEDLINE
الوصف
تدمد:2093-5978
DOI:10.3803/EnM.2023.501