ArticleJournal of bone metabolism2016
Deficiency of Lipocalin-2 Promotes Proliferation and Differentiation of Osteoclast Precursors via Regulation of c-Fms Expression and Nuclear Factor-kappa B Activation.
Article in Journal of bone metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- The impact of obesity on bone health: molecular pathways, metabolic interactions, and associated pathologies.International journal of obesity (2005) · 2026Review
- Review
- Lipocalin 2 serum levels correlate with age and bone turnover biomarkers in healthy subjects but not in postmenopausal osteoporotic women.Bone reports · 2021Article
- Genome-Wide Association Identifies Risk Pathways for SAPHO Syndrome.Frontiers in cell and developmental biology · 2021Article
- Lipocalin-2 counteracts metabolic dysregulation in obesity and diabetes.The Journal of experimental medicine · 2020Article
- Lipoteichoic Acid Accelerates Bone Healing by Enhancing Osteoblast Differentiation and Inhibiting Osteoclast Activation in a Mouse Model of Femoral Defects.International journal of molecular sciences · 2020Article
- Molecular Basis of Bone Aging.International journal of molecular sciences · 2020Review
- Hepatocyte-Derived Lipocalin 2 Is a Potential Serum Biomarker Reflecting Tumor Burden in Hepatoblastoma.The American journal of pathology · 2018Article
- The relationship among serum lipocalin 2, bone turnover markers, and bone mineral density in outpatient women.Endocrine · 2018Article
- Fexaramine Inhibits Receptor Activator of Nuclear Factor-κB Ligand-induced Osteoclast Formation via Nuclear Factor of Activated T Cells Signaling Pathways.Journal of bone metabolism · 2017Article
- Novel bone metabolism-associated hormones: the importance of the pre-analytical phase for understanding their physiological roles.Endocrine · 2017Review
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Authors and funding
8 authors at 2 institutions in 1 country.
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Abstract
backgroundLipocalin-2 (LCN2), a small glycoprotein, has a pivotal role in diverse biological processes such as cellular proliferation and differentiation. We previously reported that LCN2 is implicated in osteoclast formation induced by receptor activator of nuclear factor-kappa B ligand (RANKL) and macrophage colony-stimulating factor (M-CSF). In the present study, we used a knockout mouse model to further investigate the role of LCN2 in osteoclast development.
methodsOsteoclastogenesis was assessed using primary bone marrow-derived macrophages. RANKL and M-CSF signaling was determined by immunoblotting, cell proliferation by bromodeoxyuridine (BrdU) enzyme-linked immunosorbent assay (ELISA), and apoptosis by cell death detection ELISA. Bone morphometric parameters were determined using a micro-computed tomography system.
resultsOur results showed that LCN2 deficiency increases tartrate-resistant acid phosphatase (TRAP)-positive multinucleated osteoclast formation in vitro, a finding that reflects enhanced proliferation and differentiation of osteoclast lineage cells. LCN2 deficiency promotes M-CSF-induced proliferation of bone marrow macrophages (BMMs), osteoclast precursors, without altering their survival. The accelerated proliferation of LCN2-deficient precursors is associated with enhanced expression and activation of the M-CSF receptor, c-Fms. Furthermore, LCN2 deficiency stimulates the induction of c-Fos and nuclear factor of activated T cells c1 (NFATc1), key transcription factors for osteoclastogenesis, and promotes RANKL-induced inhibitor of kappa B (IκBα) phosphorylation. Interestingly, LCN2 deficiency does not affect basal osteoclast formation in vivo, suggesting that LCN2 might play a role in the enhanced osteoclast development that occurs under some pathological conditions.
conclusionsOur study establishes LCN2 as a negative modulator of osteoclast formation, results that are in accordance with our previous findings.
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