ArticleJournal of orthopaedic translation2022
Loss of Bcl-3 delays bone fracture healing through activating NF-κB signaling in mesenchymal stem cells.
Article in Journal of orthopaedic translation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Unveiling the multifaceted roles of BCL3: biological functions and disease implications.Apoptosis : an international journal on programmed cell death · 2026Review
- Advancements in bone organoids: perspectives on construction methodologies and application strategies.Journal of advanced research · 2026Review
- Otubain 2 stabilizes TNF‑receptor associated factor 3 to accelerate bone fracture healing.Molecular medicine reports · 2025Article
- Knockdown of LncRNA H19 inhibits vascularization and endochondral ossification via the MiRNA-21a-5p-Smad7/p-Smad2/3 pathway in fracture repair.Scientific reports · 2025Article
- Oral Citrate Supplementation Mitigates Age-Associated Pathologic Intervertebral Disc Calcification in LG/J Mice.Aging cell · 2025Article
- FKBP5 Induces Senescence in BMSCs and Inhibits Osteogenic Differentiation Through the Canonical WNT/β-Catenin Signalling Pathway in Senile Osteoporosis.Journal of cellular and molecular medicine · 2025Article
- Oral citrate supplementation mitigates age-associated pathological intervertebral disc calcification in LG/J mice.bioRxiv : the preprint server for biology · 2024Article
- IĸB Protein BCL3 as a Controller of Osteogenesis and Bone Health.Arthritis & rheumatology (Hoboken, N.J.) · 2023Article
- Targeted and responsive biomaterials in osteoarthritis.Theranostics · 2023Review
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Bone fracture healing is a postnatal regenerative process in which fibrocartilaginous callus formation and bony callus formation are important. Bony callus formation requires osteoblastic differentiation of MSCs. Materials and methods: The formation of callus was assessed by μCT, Safranin-O, H&E and Masson trichrome staining. Osteogenesis of MSCs was analyzed by ALP staining, ARS staining, qRT-PCR and WB. And we also used IF and TOP/FOP Flash luciferase reporter to assess the nuclear translocation of PP65. Results: In this study, we found Bcl-3 showed a significant correlation with bone fracture healing. Results of μCT showed that loss of Bcl-3 delays bone fracture healing. Safranin-O, H&E and Masson trichrome staining confirmed that loss of Bcl-3 impacted the formation of cartilage and woven bone in callus. Further experiments in vitro manifested that Bcl-3-knockdown could inhibit MSCs osteoblastic differentiation through releasing the inhibition on NF-κB signaling by Co-IP, IF staining and luciferase reporter assay. Conclusions: We unveiled that loss of Bcl-3 could lead to inhibited osteogenic differentiation of MSCs via promoting PP65 nuclear translocation. The translational potential of this article: Our data demonstrated that overexpression of Bcl-3 accelerates bone fracture healing, which serves as a promising therapeutic target for bone fracture treatment.
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