ArticleScientific reports2017
Small leucine rich proteoglycans, a novel link to osteoclastogenesis.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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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.
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Who cites it
25 citing papers in PubMed, 47 citations in OpenAlex.
- Osteoblast-derived osteomodulin restrains osteoclastogenesis via ITGB8/RRM2-mediated reduction of mitochondrial respiration and mitochondrial ATP production.Experimental & molecular medicine · 2026Article
- Control of tissue homeostasis by the extracellular matrix: Synthetic heparan sulfate as a promising therapeutic for periodontal health and bone regeneration.Periodontology 2000 · 2024Review
- Osteomodulin downregulation is associated with osteoarthritis development.Bone research · 2023Article
- The Landscape of Small Leucine-Rich Proteoglycan Impact on Cancer Pathogenesis with a Focus on Biglycan and Lumican.Cancers · 2023Review
- Small leucine rich proteoglycans: Biology, function and their therapeutic potential in the ocular surface.The ocular surface · 2023Review
- Synergistic effect of sulfonation followed by precipitation of amorphous calcium phosphate on the bone-bonding strength of carbon fiber reinforced polyetheretherketone.Scientific reports · 2023Article
- Systems biology approach discovers comorbidity interaction of Parkinson's disease with psychiatric disorders utilizing brain transcriptome.Frontiers in molecular neuroscience · 2023Article
- Article
- Investigation of Transcriptome Patterns in Endometrial Cancers from Obese and Lean Women.International journal of molecular sciences · 2022Article
- Integration of a miniaturized DMMB assay with high-throughput screening for identifying regulators of proteoglycan metabolism.Scientific reports · 2022Article
- Skeletal stem cell fate defects caused by Pdgfrb activating mutation.Development (Cambridge, England) · 2021Article
- Biglycan: an emerging small leucine-rich proteoglycan (SLRP) marker and its clinicopathological significance.Molecular and cellular biochemistry · 2021Review
- Lumican in Carcinogenesis-Revisited.Biomolecules · 2021Review
- Small leucine-rich proteoglycans in physiological and biomechanical function of bone.Matrix biology plus · 2021Review
- Influence of microcurrent on the modulation of remodelling genes in a wound healing assay.Molecular biology reports · 2021Article
- OPG-Fc treatment partially rescues low bone mass phenotype in mature Bgn/Fmod deficient mice but is deleterious to the young mouse skeleton.Journal of structural biology · 2020Article
- Biglycan and chondroitin sulfate play pivotal roles in bone toughness via retaining bound water in bone mineral matrix.Matrix biology : journal of the International Society for Matrix Biology · 2020Article
- Communications via the Small Leucine-rich Proteoglycans: Molecular Specificity in Inflammation and Autoimmune Diseases.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2020Review
- Biglycan in the Skeleton.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2020Review
- Collagen VIα2 chain deficiency causes trabecular bone loss by potentially promoting osteoclast differentiation through enhanced TNFα signaling.Scientific reports · 2020Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Biglycan (Bgn) and Fibromodulin (Fmod) are subtypes of the small leucine-rich family of proteoglycans (SLRP). In this study we examined the skeletal phenotype of BgnFmod double knockout (BgnFmod KO) mice and found they were smaller in size and have markedly reduced bone mass compared to WT. The low bone mass (LBM) phenotype is the result of both the osteoblasts and osteoclasts from BgnFmod KO mice having higher differentiation potential and being more active compared to WT mice. Using multiple approaches, we showed that both Bgn and Fmod directly bind TNFα as well as RANKL in a dose dependent manner and that despite expressing higher levels of both TNFα and RANKL, BgnFmod KO derived osteoblasts cannot retain these cytokines in the vicinity of the cells, which leads to elevated TNFα and RANKL signaling and enhanced osteoclastogenesis. Furthermore, adding either Bgn or Fmod to osteoclast precursor cultures significantly attenuated the cells ability to form TRAP positive, multinucleated giant cells. In summary, our data indicates that Bgn and Fmod expressed by the bone forming cells, are novel coupling ECM components that control bone mass through sequestration of TNFα and/or RANKL, thereby adjusting their bioavailability in order to regulate osteoclastogenesis.
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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.