ArticleBone2014
Runx2 is required for early stages of endochondral bone formation but delays final stages of bone repair in Axin2-deficient mice.
Article in Bone, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 52 citations in OpenAlex.
- Evidence for Altered Canonical Wnt Signaling in the Trabecular Bone of Elderly Postmenopausal Women with Fragility Femoral Fracture.BioMed research international · 2016Trial
- Bifidobacterium longum subsp. infantis CCFM1445 Promotes Bone Growth in Growing Mice Via Modulating Gut Microbiota and Arginine Metabolism Pathway.Probiotics and antimicrobial proteins · 2026Article
- Biological processes and factors involved in soft and hard tissue healing.Periodontology 2000 · 2025Review
- Article
- Decoding Cold Therapy Mechanisms of Enhanced Bone Repair through Sensory Receptors and Molecular Pathways.Biomedicines · 2024Article
- Predictive value of preoperative Fried Frailty Phenotype assessment and serum biomarkers on the prognosis of elderly patients with femoral neck fracture under general anesthesia within 3 months after surgery.Turkish journal of medical sciences · 2024Article
- Article
- Craniofacial dysmorphology in Down syndrome is caused by increased dosage of Dyrk1a and at least three other genes.Development (Cambridge, England) · 2023Article
- Instructive cartilage regeneration modalities with advanced therapeutic implantations under abnormal conditions.Bioactive materials · 2022Review
- Genetic profiling of human bone marrow and adipose tissue-derived mesenchymal stem cells reveals differences in osteogenic signaling mediated by graphene.Journal of nanobiotechnology · 2021Article
- Article
- The potential function of miR-135b-mediated JAK2/STAT3 signaling pathway during osteoblast differentiation.The Kaohsiung journal of medical sciences · 2020Article
- RUNX2-modifying enzymes: therapeutic targets for bone diseases.Experimental & molecular medicine · 2020Review
- Deficiency in the phosphatase PHLPP1 suppresses osteoclast-mediated bone resorption and enhances bone formation in mice.The Journal of biological chemistry · 2019Article
- MicroRNA-153 inhibits cell proliferation, migration, invasion and epithelial-mesenchymal transition in breast cancer via direct targeting of RUNX2.Experimental and therapeutic medicine · 2019Article
- Peroxisome Proliferator-Activated Receptor-γ Knockdown Impairs Bone Morphogenetic Protein-2-Induced Critical-Size Bone Defect Repair.The American journal of pathology · 2019Article
- Cellular biology of fracture healing.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2019Review
- Tanshinone IIA promotes osteogenic differentiation of human periodontal ligament stem cells via ERK1/2-dependent Runx2 induction.American journal of translational research · 2019Article
- Clinical and radiological findings in a severe case of cleidocranial dysplasia.BMJ case reports · 2018Article
- Histone Deacetylase 3 Deletion in Mesenchymal Progenitor Cells Hinders Long Bone Development.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2017Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
Abstract
Runx2 and Axin2 regulate skeletal development. We recently determined that Axin2 and Runx2 molecularly interact in differentiating osteoblasts to regulate intramembranous bone formation, but the relationship between these factors in endochondral bone formation was unresolved. To address this, we examined the effects of Axin2 deficiency on the cleidocranial dysplasia (CCD) phenotype of Runx2(+/-) mice, focusing on skeletal defects attributed to improper endochondral bone formation. Axin2 deficiency unexpectedly exacerbated calvarial components of the CCD phenotype in the Runx2(+/-) mice; the endocranial layer of the frontal suture, which develops by endochondral bone formation, failed to mineralize in Axin2(-/-):Runx2(+/-) mice, resulting in a cartilaginous, fibrotic and larger fontanel than observed in Runx2(+/-) mice. Transcripts associated with cartilage development (e.g., Acan, miR140) were expressed at higher levels, whereas blood vessel morphogenesis transcripts (e.g., Slit2) were suppressed in Axin2(-/-):Runx2(+/-) calvaria. Cartilage maturation was impaired, as primary chondrocytes from double mutant mice demonstrated delayed differentiation and produced less calcified matrix in vitro. The genetic dominance of Runx2 was also reflected during endochondral fracture repair, as both Runx2(+/-) and double mutant Axin2(-/-):Runx2(+/-) mice had enlarged fracture calluses at early stages of healing. However, by the end stages of fracture healing, double mutant animals diverged from the Runx2(+/-) mice, showing smaller calluses and increased torsional strength indicative of more rapid end stage bone formation as seen in the Axin2(-/-) mice. Taken together, our data demonstrate a dominant role for Runx2 in chondrocyte maturation, but implicate Axin2 as an important modulator of the terminal stages of endochondral bone formation.
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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.