ArticleJournal of cell science2013
Fibrillin-1 directly regulates osteoclast formation and function by a dual mechanism.
Article in Journal of cell science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- Endothelial BMAL1 decline during aging leads to bone loss by destabilizing extracellular fibrillin-1.The Journal of clinical investigation · 2024Article
- Tissue material properties, whole-bone morphology and mechanical behavior in theMatrix biology plus · 2024Article
- Proteomics Sequencing Reveals the Role of TGF-β Signaling Pathway in the Peripheral Blood of Offspring Rats Exposed to Fluoride.Biological trace element research · 2024Article
- Extracellular Vesicle Protein Expression in Doped Bioactive Glasses: Further Insights Applying Anomaly Detection.International journal of molecular sciences · 2024Article
- Pyrroloquinoline quinone alleviates natural aging-related osteoporosis via a novel MCM3-Keap1-Nrf2 axis-mediated stress response and Fbn1 upregulation.Aging cell · 2023Article
- Article
- The extracellular matrix glycoprotein fibrillin-1 in health and disease.Frontiers in cell and developmental biology · 2023Review
- CD34Cellular and molecular life sciences : CMLS · 2022Article
- The Multiple Functions of Fibrillin-1 Microfibrils in Organismal Physiology.International journal of molecular sciences · 2022Review
- Article
- Human perivascular stem cells prevent bone graft resorption in osteoporotic contexts by inhibiting osteoclast formation.Stem cells translational medicine · 2020Article
- Fibrillin-1 and fibrillin-1-derived asprosin in adipose tissue function and metabolic disorders.Journal of cell communication and signaling · 2020Review
- Marfan syndrome; A connective tissue disease at the crossroads of mechanotransduction, TGFβ signaling and cell stemness.Matrix biology : journal of the International Society for Matrix Biology · 2018Review
- Transglutaminase activity regulates differentiation, migration and fusion of osteoclasts via affecting actin dynamics.Journal of cellular physiology · 2018Article
- Inhibition of osteoclastogenesis by stem cell-derived extracellular matrix through modulation of intracellular reactive oxygen species.Acta biomaterialia · 2018Article
- Osteoactivin inhibition of osteoclastogenesis is mediated through CD44-ERK signaling.Experimental & molecular medicine · 2016Article
- The protocol for the isolation and cryopreservation of osteoclast precursors from mouse bone marrow and spleen.Cytotechnology · 2016Article
- Fibrillin microfibrils in bone physiology.Matrix biology : journal of the International Society for Matrix BiologyReview
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Mutations in the fibrillin-1 gene give rise to a number of heritable disorders, which are all characterized by various malformations of bone as well as manifestations in other tissues. However, the role of fibrillin-1 in the development and homeostasis of bone is not well understood. Here, we examined the role of fibrillin-1 in regulating osteoclast differentiation from primary bone-marrow-derived precursors and monocytic RAW 264.7 cells. The soluble N-terminal half of fibrillin-1 (rFBN1-N) strongly inhibited osteoclastogenesis, whereas the C-terminal half (rFBN1-C) did not. By contrast, when rFBN1-N was immobilized on calcium phosphate, it did not affect osteoclastogenesis but modulated osteoclast resorptive activity, which was evident by a larger number of smaller resorption pits. Using a panel of recombinant sub-fragments spanning rFBN1-N, we localized an osteoclast inhibitory activity to the 63 kDa subfragment rF23 comprising the N-terminal region of fibrillin-1. Osteoclastic resorption led to the generation of small fibrillin-1 fragments that were similar to those identified in human vertebral bone extracts. rF23, but not rFBN1-N, was found to inhibit the expression of cathepsin K, matrix metalloproteinase 9 and Dcstamp in differentiating osteoclasts. rFBN1-N, but not rF23, exhibited interaction with RANKL. Excess RANKL rescued the inhibition of osteoclastogenesis by rFBN1-N. By contrast, rF23 disrupted RANKL-induced Ca(2+) signaling and activation of transcription factor NFATc1. These studies highlight a direct dual inhibitory role of N-terminal fibrillin-1 fragments in osteoclastogenesis, the sequestration of RANKL and the inhibition of NFATc1 signaling, demonstrating that osteoclastic degradation of fibrillin-1 provides a potent negative feedback that limits osteoclast formation and function.
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Registered trials
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