ArticleScientific reports2020
Collagen VIα2 chain deficiency causes trabecular bone loss by potentially promoting osteoclast differentiation through enhanced TNFα signaling.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- COL6A2 in clear cell renal cell carcinoma: a multifaceted driver of tumor progression, immune evasion, and drug sensitivity.Journal of translational medicine · 2025Article
- Collagen type VI regulates TGF-β bioavailability in skeletal muscle in mice.The Journal of clinical investigation · 2025Article
- Whole-exome sequencing and copy number alterations analysis in a case of expansive florid cemento-osseous dysplasia.Clinical case reports · 2024Article
- Type VI Collagen Deficiency Causes Enhanced Periodontal Tissue Destruction.Journal of dental research · 2024Article
- Collagen VI in the Musculoskeletal System.International journal of molecular sciences · 2023Review
- The Role of Type VI Collagen in Alveolar Bone.International journal of molecular sciences · 2022Article
- Type VI Collagen Regulates Endochondral Ossification in the Temporomandibular Joint.JBMR plus · 2022Article
- Coordinate roles for collagen VI and biglycan in regulating tendon collagen fibril structure and function.Matrix biology plus · 2022Article
- Analysis of the cells isolated from epithelial cell rests of Malassez through single-cell limiting dilution.Scientific reports · 2022Article
- Tryptophan and Kynurenine Enhances the Stemness and Osteogenic Differentiation of Bone Marrow-Derived Mesenchymal Stromal Cells In Vitro and In Vivo.Materials (Basel, Switzerland) · 2021Article
- Collagen VI Muscle Disorders: Mutation Types, Pathogenic Mechanisms and Approaches to Therapy.Advances in experimental medicine and biology · 2021Article
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Type VI collagen is well known for its role in muscular disorders, however its function in bone is still not well understood. To examine its role in bone we analyzed femoral and vertebral bone mass by micro-computed tomography analysis, which showed lower bone volume/total volume and trabecular number in Col6α2-KO mice compared with WT. Dynamic histomorphometry showed no differences in trabecular bone formation between WT and Col6α2-KO mice based on the mineral appositional rate, bone formation rate, and mineralizing perimeter. Femoral sections were assessed for the abundance of Tartrate Resistant Acid Phosphatase-positive osteoclasts, which revealed that mutant mice had more osteoclasts compared with WT mice, indicating that the primary effect of Col6a2 deficiency is on osteoclastogenesis. When bone marrow stromal cells (BMSCs) from WT and Col6α2-KO mice were treated with rmTNFα protein, the Col6α2-KO cells expressed higher levels of TNFα mRNA compared with WT cells. This was accompanied by higher levels of p-p65, a down-stream target of TNFα, suggesting that BMSCs from Col6α2-KO mice are highly sensitive to TNFα signaling. Taken together, our data imply that Col6a2 deficiency causes trabecular bone loss by enhancing osteoclast differentiation through enhanced TNFα signaling.
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