ArticleThe Journal of biological chemistry2014
Vinculin regulates osteoclast function.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 47 citations in OpenAlex.
- Engineered Poly (amino acid) Hydrogel Synchronizes Sequential Infection Elimination and Osteogenic Activation for Single-stage Reconstruction of Infected Bone Defects.Theranostics · 2026Article
- Structure and function of the membrane microdomains in osteoclasts.Bone research · 2023Review
- The role of TRPV2 as a regulator on the osteoclast differentiation during orthodontic tooth movement in rats.Scientific reports · 2023Article
- The checkpoint inhibitor PD-1H/VISTA controls osteoclast-mediated multiple myeloma bone disease.Nature communications · 2023Article
- Cell-scaffold interactions in tissue engineering for oral and craniofacial reconstruction.Bioactive materials · 2023Article
- Porphyromonas gingivalis induction of TLR2 association with Vinculin enables PI3K activation and immune evasion.PLoS pathogens · 2023Article
- Roles of focal adhesion proteins in skeleton and diseases.Acta pharmaceutica Sinica. B · 2023Review
- Potential mechanisms of osteoprotegerin-induced damage to osteoclast adhesion structures via P2X7R-mediated MAPK signaling.International journal of molecular medicine · 2022Article
- Expression of the phagocytic receptors αFrontiers in immunology · 2022Article
- LncRNA-mRNA Expression Profiles of Osteoclast After Conditional Knockout HIF-1α.Frontiers in genetics · 2022Article
- Epigenetic DNA Methylation Signatures Associated With the Severity of Paget's Disease of Bone.Frontiers in cell and developmental biology · 2022Article
- Heterogeneity and Actin Cytoskeleton in Osteoclast and Macrophage Multinucleation.International journal of molecular sciences · 2020Review
- Context-Dependent Role of Vinculin in Neutrophil Adhesion, Motility and Trafficking.Scientific reports · 2020Article
- Regulation of Osteoclast Differentiation at Multiple Stages by Protein Kinase D Family Kinases.International journal of molecular sciences · 2020Article
- PIP5k1β controls bone homeostasis through modulating both osteoclast and osteoblast differentiation.Journal of molecular cell biology · 2020Article
- Bone morphogenetic proteins: Their role in regulating osteoclast differentiation.Bone reports · 2019Review
- Non-canonical Wnt signals regulate cytoskeletal remodeling in osteoclasts.Cellular and molecular life sciences : CMLS · 2018Review
- The Actin-Binding Protein PPP1r18 Regulates Maturation, Actin Organization, and Bone Resorption Activity of Osteoclasts.Molecular and cellular biology · 2018Article
- A 15-amino acid C-terminal peptide of beta-defensin-3 inhibits bone resorption by inhibiting the osteoclast differentiation and disrupting podosome belt formation.Journal of molecular medicine (Berlin, Germany) · 2017Article
- Serotonin-reuptake inhibitors act centrally to cause bone loss in mice by counteracting a local anti-resorptive effect.Nature medicine · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Osteoclastic bone resorption depends upon the cell's ability to organize its cytoskeleton. Because vinculin (VCL) is an actin-binding protein, we asked whether it participates in skeletal degradation. Thus, we mated VCL(fl/fl) mice with those expressing cathepsin K-Cre (CtsK-VCL) to delete the gene in mature osteoclasts or lysozyme M-Cre (LysM-VCL) to target all osteoclast lineage cells. VCL-deficient osteoclasts differentiate normally but, reflecting cytoskeletal disorganization, form small actin rings and fail to effectively resorb bone. In keeping with inhibited resorptive function, CtsK-VCL and LysM-VCL mice exhibit a doubling of bone mass. Despite cytoskeletal disorganization, the capacity of VCL(-/-) osteoclastic cells to normally phosphorylate c-Src in response to αvβ3 integrin ligand is intact. Thus, integrin-activated signals are unrelated to the means by which VCL organizes the osteoclast cytoskeleton. WT VCL completely rescues actin ring formation and bone resorption, as does VCL(P878A), which is incapable of interacting with Arp2/3. As expected, deletion of the VCL tail domain (VCL(1-880)), which binds actin, does not normalize VCL(-/-) osteoclasts. The same is true regarding VCL(I997A), which also prevents VCL/actin binding, and VCL(A50I) and VCL(811-1066), both of which arrest talin association. Thus, VCL binding talin, but not Arp2/3, is critical for osteoclast function, and its selective inhibition retards physiological bone loss.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.