ArticleThe American journal of pathology2014
Mutation in osteoactivin decreases bone formation in vivo and osteoblast differentiation in vitro.
Article in The American journal of pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 61 citations in OpenAlex.
- Article
- Genetic subtraction reveals divergent pathways and targets in anxiety-related and anxiety-independent TMD.The journal of headache and pain · 2026Article
- Fabrication and Evaluation of Thermoresponsive GPNMB-Hydrogels as an Innovative Osteogenic Therapeutic Strategy.Pharmaceutical research · 2025Article
- Parathyroid Hormone as a Modulator of Skeletal Muscle: Insights into Bone-Muscle and Nerve-Muscle Interactions.International journal of molecular sciences · 2025Review
- Preparation of genetically or chemically engineered exosomes and their therapeutic effects in bone regeneration and anti-inflammation.Frontiers in bioengineering and biotechnology · 2024Review
- Inhibition of EGFR Pathway Suppresses M1 Macrophage Polarization and Osteoclastogenesis, Mitigating Titanium Particle-Induced Bone Resorption.Journal of inflammation research · 2024Article
- The Lymphatic Endothelial Cell Secretome Inhibits Osteoblast Differentiation and Bone Formation.Cells · 2023Article
- Conditional Loss of Nmp4 in Mesenchymal Stem Progenitor Cells Enhances PTH-Induced Bone Formation.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2023Article
- Stromal niche inflammation mediated by IL-1 signalling is a targetable driver of haematopoietic ageing.Nature cell biology · 2023Article
- Improved Protocol to Study Osteoblast and Adipocyte Differentiation Balance.Biomedicines · 2022Article
- Osteopathy in Complex Lymphatic Anomalies.International journal of molecular sciences · 2022Review
- Transcriptome of HPβCD-treated Niemann-Pick disease type C1 cells highlights GPNMB as a biomarker for therapeutics.Human molecular genetics · 2021Article
- Quantitative trait locus mapping identifies the Gpnmb gene as a modifier of mouse macrophage lysosome function.Scientific reports · 2021Article
- The soluble glycoprotein NMB (GPNMB) produced by macrophages induces cancer stemness and metastasis via CD44 and IL-33.Cellular & molecular immunology · 2021Article
- Glycoprotein nonmetastatic melanoma protein B: A key mediator and an emerging therapeutic target in autoimmune diseases.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Review
- GPNMB contributes to a vicious circle for chronic obstructive pulmonary disease.Bioscience reports · 2020Review
- Microglia express GPNMB in the brains of Alzheimer's disease and Nasu-Hakola disease.Intractable & rare diseases research · 2019Article
- The suppressive effects of miR-508-5p on the odontogenic differentiation of human dental pulp stem cells by targeting glycoprotein non-metastatic melanomal protein B.Stem cell research & therapy · 2019Article
- Glycoprotein NMB: an Emerging Role in Neurodegenerative Disease.Molecular neurobiology · 2018Review
- Screening Gene Knockout Mice for Variation in Bone Mass: Analysis by μCT and Histomorphometry.Current osteoporosis reports · 2018Review
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
We have previously identified osteoactivin (OA), encoded by Gpnmb, as an osteogenic factor that stimulates osteoblast differentiation in vitro. To elucidate the importance of OA in osteogenesis, we characterized the skeletal phenotype of a mouse model, DBA/2J (D2J) with a loss-of-function mutation in Gpnmb. Microtomography of D2J mice showed decreased trabecular mass, compared to that in wild-type mice [DBA/2J-Gpnmb(+)/SjJ (D2J/Gpnmb(+))]. Serum analysis showed decreases in OA and the bone-formation markers alkaline phosphatase and osteocalcin in D2J mice. Although D2J mice showed decreased osteoid and mineralization surfaces, their osteoblasts were increased in number, compared to D2J/Gpnmb(+) mice. We then examined the ability of D2J osteoblasts to differentiate in culture, where their differentiation and function were decreased, as evidenced by low alkaline phosphatase activity and matrix mineralization. Quantitative RT-PCR analyses confirmed the decreased expression of differentiation markers in D2J osteoblasts. In vitro, D2J osteoblasts proliferated and survived significantly less, compared to D2J/Gpnmb(+) osteoblasts. Next, we investigated whether mutant OA protein induces endoplasmic reticulum stress in D2J osteoblasts. Neither endoplasmic reticulum stress markers nor endoplasmic reticulum ultrastructure were altered in D2J osteoblasts. Finally, we assessed underlying mechanisms that might alter proliferation of D2J osteoblasts. Interestingly, TGF-β receptors and Smad-2/3 phosphorylation were up-regulated in D2J osteoblasts, suggesting that OA contributes to TGF-β signaling. These data confirm the anabolic role of OA in postnatal bone formation.
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