ArticleThe Journal of biological chemistry2013
CCN3 protein participates in bone regeneration as an inhibitory factor.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 65 citations in OpenAlex.
- Hypothalamic prolactin receptorNature communications · 2026Article
- Cell Supported Single Membrane Technique for the Treatment of Large Bone Defects: Depletion of CD8Cells · 2026Article
- Critical Requirement of Senescence-Associated CCN3 Expression in CD44-Positive Stem Cells for Osteoarthritis Progression.International journal of molecular sciences · 2025Article
- Dynamic changes in Ccn3 expression across the limbic forebrain through the mouse estrous cycle and during lactation.Journal of neuroendocrinology · 2025Article
- Epitenon-derived progenitors drive fibrosis and regeneration after flexor tendon injury in a spatially-dependent manner.Nature communications · 2025Article
- CCN Proteins as Matricellular Regulators of Bone in Aging and Disease.Current osteoporosis reports · 2025Review
- Exploring the Role of Ccn3 in Type III Cell of Mice Taste Buds.Journal of neurochemistry · 2025Article
- Article
- A maternal brain hormone that builds bone.Nature · 2024Article
- Design, synthesis and biological evaluation of novel pyrimidine derivatives as bone anabolic agents promoting osteogenesisRSC medicinal chemistry · 2024Article
- Cellular plasticity of the bone marrow niche promotes hematopoietic stem cell regeneration.Nature genetics · 2023Article
- Single-Cell RNA-Sequencing Reveals the Skeletal Cellular Dynamics in Bone Repair and Osteoporosis.International journal of molecular sciences · 2023Review
- Temperal and spatial expression of CCN1, CCN3, CCN4, CCN5 and CCN6 proteins in the developing postnatal teeth.Journal of cell communication and signaling · 2023Article
- Structural insights into regulation of CCN protein activities and functions.Journal of cell communication and signaling · 2023Review
- The regulation and functions of the matricellular CCN proteins induced by shear stress.Journal of cell communication and signaling · 2023Review
- Myeloid CCN3 protects against aortic valve calcification.Cell communication and signaling : CCS · 2023Article
- Single-cell atlas of craniogenesis uncovers SOXC-dependent, highly proliferative, and myofibroblast-like osteodermal progenitors.Cell reports · 2022Article
- Pathological differences in the bone healing processes between tooth extraction socket and femoral fracture.Bone reports · 2022Article
- Molecular and Genetic Interactions between CCN2 and CCN3 behind Their Yin-Yang Collaboration.International journal of molecular sciences · 2022Review
- Cellular communication network factor 3 in cartilage development and maintenance.Journal of cell communication and signaling · 2021Review
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CCN3, a member of the CCN protein family, inhibits osteoblast differentiation in vitro. However, the role of CCN3 in bone regeneration has not been well elucidated. In this study, we investigated the role of CCN3 in bone regeneration. We identified the Ccn3 gene by microarray analysis as a highly expressed gene at the early phase of bone regeneration in a mouse bone regeneration model. We confirmed the up-regulation of Ccn3 at the early phase of bone regeneration by RT-PCR, Western blot, and immunofluorescence analyses. Ccn3 transgenic mice, in which Ccn3 expression was driven by 2.3-kb Col1a1 promoter, showed osteopenia compared with wild-type mice, but Ccn3 knock-out mice showed no skeletal changes compared with wild-type mice. We analyzed the bone regeneration process in Ccn3 transgenic mice and Ccn3 knock-out mice by microcomputed tomography and histological analyses. Bone regeneration in Ccn3 knock-out mice was accelerated compared with that in wild-type mice. The mRNA expression levels of osteoblast-related genes (Runx2, Sp7, Col1a1, Alpl, and Bglap) in Ccn3 knock-out mice were up-regulated earlier than those in wild-type mice, as demonstrated by RT-PCR. Bone regeneration in Ccn3 transgenic mice showed no significant changes compared with that in wild-type mice. Phosphorylation of Smad1/5 was highly up-regulated at bone regeneration sites in Ccn3 KO mice compared with wild-type mice. These results indicate that CCN3 is up-regulated in the early phase of bone regeneration and acts as a negative regulator for bone regeneration. This study may contribute to the development of new strategies for bone regeneration therapy.
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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 Socratic graph.