ArticleCell proliferation2019
TGF-β1 promotes gap junctions formation in chondrocytes via Smad3/Smad4 signalling.
Article in Cell proliferation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Nasal Chondrocytes Intensively Invade and Repair Pathologically Altered Cartilage Through Intrinsic Genomic Mechanisms: A Narrative Review.Current rheumatology reviews · 2026Review
- Gene replacement therapy for Piga GPI-anchor deficiency in the developing nervous system.bioRxiv : the preprint server for biology · 2025Article
- Up IGF-I via high-toughness adaptive hydrogels for remodeling growth plate of children.Regenerative biomaterials · 2025Article
- Reduced Cell Migration in Human Chondrocyte Sheets Increases Tissue Stiffness and Cartilage Protein Production.Tissue engineering and regenerative medicine · 2024Article
- Advancing skeletal health and disease research with single-cell RNA sequencing.Military Medical Research · 2024Review
- Role of transforming growth factor-β in peripheral nerve regeneration.Neural regeneration research · 2024Review
- Platelet-derived growth factor PDGF-AA upregulates connexin 43 expression and promotes gap junction formations in osteoblast cells throughBiochemistry and biophysics reports · 2023Article
- Cyclic di-adenosine monophosphate regulates the osteogenic and adipogenic differentiation of hPDLSCs via MAPK and NF-κB signaling.Acta biochimica et biophysica Sinica · 2023Article
- The role of TGF-beta3 in cartilage development and osteoarthritis.Bone research · 2023Review
- miR-29b inhibits TGF-β1-induced cell proliferation in articular chondrocytes.Biochemistry and biophysics reports · 2022Article
- Valproic acid enhances neurosphere formation in cultured rat embryonic cortical cells through TGFβ1 signaling.Journal of biomedical research · 2022Article
- Naringin in the repair of knee cartilage injury via the TGF-β/ALK5/Smad2/3 signal transduction pathway combined with an acellular dermal matrix.Journal of orthopaedic translation · 2022Article
- SMAD4 contributes to chondrocyte and osteocyte development.Journal of cellular and molecular medicine · 2022Review
- Expression and Regulatory Network Analysis of BICC1 for Aged Sca-1-Positive Bone Narrow Mesenchymal Stem Cells.Disease markers · 2022Article
- The role of TGF-β2 in cartilage development and diseases.Bone & joint research · 2021Article
- Transforming growth factor-β1-induced N-cadherin drives cell-cell communication through connexin43 in osteoblast lineage.International journal of oral science · 2021Article
- CTGF facilitates cell-cell communication in chondrocytes via PI3K/Akt signalling pathway.Cell proliferation · 2021Article
- Gap junction-mediated cell-to-cell communication in oral development and oral diseases: a concise review of research progress.International journal of oral science · 2020Review
- [Metformin inhibits collagen production in rat biliary fibroblasts: the molecular signaling mechanism].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020Article
- Blocking Connexin-43 mediated hemichannel activity protects against early tubular injury in experimental chronic kidney disease.Cell communication and signaling : CCS · 2020Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
objectivesConnexin-mediated functional gap junction intercellular communication (GJIC) has a vital role in development, homeostasis and pathology. Transforming growth factor-β1 (TGF-β1), as one of the most vital factors in chondrocytes, promotes cartilage precursor cell differentiation and chondrocyte proliferation, migration and metabolism. However, how TGF-β1 mediates GJIC in chondrocytes remains unclear. This study aims to determine the influence of TGF-β1 on GJIC in mouse chondrocytes and its underlying mechanism.
methodsqPCR and mRNA microarray were used to verify the expression of genes in the TGF-β and connexin families in cartilage and chondrocytes. A scrape loading/dye transfer assay was performed to explore GJIC. Western blot analysis was used to detect connexin43 (Cx43) and Smad signalling components. Immunofluorescence staining was performed to characterize protein distribution.
resultsThe TGF-β1 mRNA was the highest expressed member of the TGFβ super family in cartilage. TGF-β1 promoted functional GJIC through increased expression of Cx43. TGF-β1-mediated GJIC required the participation of TGF-β type I receptor. TGF-β1 activated Smad3 and Smad4 signalling to facilitate their nuclear translocation. The Smad3 and Smad4 signalling proteins bound to the promoter of Gja1 and thus initiated Cx43 gene expression.
conclusionsFor the first time, these results revealed a vital role of TGF-β1 in cell-cell communication in chondrocytes via gap junction formation. We describe the regulatory mechanism, the involvement of TGF-β type I receptor and the nuclear translocation of Smad3/4.
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