ArticlePloS one2012
Targeted overexpression of osteoactivin in cells of osteoclastic lineage promotes osteoclastic resorption and bone loss in mice.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- The janus-faced biology of GPNMB: from tissue homeostasis to cancer pathogenesis.Frontiers in molecular biosciences · 2025Review
- GPNMB-Positive Cells in Head and Neck Squamous Cell Carcinoma-Their Roles in Cancer Stemness, Therapy Resistance, and Metastasis.Pathology oncology research : POR · 2022Article
- Functional Domains and Evolutionary History of the PMEL and GPNMB Family Proteins.Molecules (Basel, Switzerland) · 2021Article
- Quantitative trait locus mapping identifies the Gpnmb gene as a modifier of mouse macrophage lysosome function.Scientific reports · 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
- Loss of GPNMB Causes Autosomal-Recessive Amyloidosis Cutis Dyschromica in Humans.American journal of human genetics · 2018Article
- Muscle-Bone Crosstalk: Emerging Opportunities for Novel Therapeutic Approaches to Treat Musculoskeletal Pathologies.Biomedicines · 2017Review
- Osteoactivin inhibition of osteoclastogenesis is mediated through CD44-ERK signaling.Experimental & molecular medicine · 2016Article
- Article
- Transgenic Expression of Osteoactivin/gpnmb Enhances Bone Formation In Vivo and Osteoprogenitor Differentiation Ex Vivo.Journal of cellular physiology · 2016Article
- GPNMB cooperates with neuropilin-1 to promote mammary tumor growth and engages integrin α5β1 for efficient breast cancer metastasis.Oncogene · 2015Article
- Mutation in Osteoactivin Promotes Receptor Activator of NFκB Ligand (RANKL)-mediated Osteoclast Differentiation and Survival but Inhibits Osteoclast Function.The Journal of biological chemistry · 2015Article
- Effects of GPNMB on proliferation and odontoblastic differentiation of human dental pulp cells.International journal of clinical and experimental pathology · 2015Article
- Mutation in osteoactivin decreases bone formation in vivo and osteoblast differentiation in vitro.The American journal of pathology · 2014Article
- Article
- Glycoprotein non-metastatic b (GPNMB): A metastatic mediator and emerging therapeutic target in cancer.OncoTargets and therapy · 2013Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
This study sought to test whether targeted overexpression of osteoactivin (OA) in cells of osteoclastic lineage, using the tartrate-resistant acid phosphase (TRAP) exon 1B/C promoter to drive OA expression, would increase bone resorption and bone loss in vivo. OA transgenic osteoclasts showed ∼2-fold increases in OA mRNA and proteins compared wild-type (WT) osteoclasts. However, the OA expression in transgenic osteoblasts was not different. At 4, 8, and 15.3 week-old, transgenic mice showed significant bone loss determined by pQCT and confirmed by μ-CT. In vitro, transgenic osteoclasts were twice as large, had twice as much TRAP activity, resorbed twice as much bone matrix, and expressed twice as much osteoclastic genes (MMP9, calciton receptor, and ADAM12), as WT osteoclasts. The siRNA-mediated suppression of OA expression in RAW264.7-derived osteoclasts reduced cell size and osteoclastic gene expression. Bone histomorphometry revealed that transgenic mice had more osteoclasts and osteoclast surface. Plasma c-telopeptide (a resorption biomarker) measurements confirmed an increase in bone resorption in transgenic mice in vivo. In contrast, histomorphometric bone formation parameters and plasma levels of bone formation biomarkers (osteocalcin and pro-collagen type I N-terminal peptide) were not different between transgenic mice and WT littermates, indicating the lack of bone formation effects. In conclusion, this study provides compelling in vivo evidence that osteoclast-derived OA is a novel stimulator of osteoclast activity and bone resorption.
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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.