ArticleInternational journal of oral science2021
Transforming growth factor-β1-induced N-cadherin drives cell-cell communication through connexin43 in osteoblast lineage.
Article in International journal of oral science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 29 citations in OpenAlex.
- Tumor Electric Field Therapy Inhibits TGF-β/C1R Signaling Axis-Driven Epithelial-Mesenchymal Transition in Glioblastoma.CNS neuroscience & therapeutics · 2026Article
- The interplay of estrogen, gut microbiome, and bone immunity in osteoporosis.Cell communication and signaling : CCS · 2025Review
- Ferulic Acid Alleviates Inflammation and Promotes Osteogenic Differentiation in Periodontitis by Inhibiting NF-Stem cells international · 2025Article
- Exploring the Mechanism of Action of Berberine on Arrhythmia After Myocardial Infarction: A Network Pharmacology, Molecular Docking, and Cellular Experimental Study.Cardiovascular therapeutics · 2025Article
- Understanding the Role of Connexins in Hepatocellular Carcinoma: Molecular and Prognostic Implications.Cancers · 2024Review
- METTL3-mediated m6A modification increases Hspa1a stability to inhibit osteoblast aging.Cell death discovery · 2024Article
- Intercellular Communication in Airway Epithelial Cell Regeneration: Potential Roles of Connexins and Pannexins.International journal of molecular sciences · 2023Review
- Annexin A5 derived from matrix vesicles protects against osteoporotic bone loss via mineralization.Bone research · 2023Article
- Review
- Circulating macrophages as the mechanistic link between mosaic loss of Y-chromosome and cardiac disease.Cell & bioscience · 2023Article
- Platelet-derived growth factor PDGF-AA upregulates connexin 43 expression and promotes gap junction formations in osteoblast cells throughBiochemistry and biophysics reports · 2023Article
- FGF19 increases mitochondrial biogenesis and fusion in chondrocytes via the AMPKα-p38/MAPK pathway.Cell communication and signaling : CCS · 2023Article
- SDF-1α Promotes Chondrocyte Autophagy through CXCR4/mTOR Signaling Axis.International journal of molecular sciences · 2023Article
- The roles of connexins and gap junctions in the progression of cancer.Cell communication and signaling : CCS · 2023Review
- The role of TGF-beta3 in cartilage development and osteoarthritis.Bone research · 2023Review
- Dynamics of Connexin 43 Down Modulation in Human Articular Chondrocytes Stimulated by Tumor Necrosis Factor Alpha.International journal of molecular sciences · 2022Article
- Connexin 43 Hemichannels Regulate Osteoblast to Osteocyte Differentiation.Frontiers in cell and developmental biology · 2022Article
- FGF7-induced E11 facilitates cell-cell communication through connexin43.International journal of biological sciences · 2021Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gap junction (GJ) has been indicated to have an intimate correlation with adhesion junction. However, the direct interaction between them partially remains elusive. In the current study, we aimed to elucidate the role of N-cadherin, one of the core components in adhesion junction, in mediating connexin 43, one of the functional constituents in gap junction, via transforming growth factor-β1(TGF-β1) induction in osteoblasts. We first elucidated the expressions of N-cadherin induced by TGF-β1 and also confirmed the upregulation of Cx43, and the enhancement of functional gap junctional intercellular communication (GJIC) triggered by TGF-β1 in both primary osteoblasts and MC3T3 cell line. Colocalization analysis and Co-IP experimentation showed that N-cadherin interacts with Cx43 at the site of cell-cell contact. Knockdown of N-cadherin by siRNA interference decreased the Cx43 expression and abolished the promoting effect of TGF-β1 on Cx43. Functional GJICs in living primary osteoblasts and MC3T3 cell line were also reduced. TGF-β1-induced increase in N-cadherin and Cx43 was via Smad3 activation, whereas knockdown of Smad3 signaling by using siRNA decreased the expressions of both N-cadherin and Cx43. Overall, these data indicate the direct interactions between N-cadherin and Cx43, and reveal the intervention of adhesion junction in functional gap junction in living osteoblasts.
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