ArticleCell death discovery2019
TGF-β1 facilitates cell-cell communication in osteocytes via connexin43- and pannexin1-dependent gap junctions.
Article in Cell death discovery, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 33 citations in OpenAlex.
- TGF-β2 enhances nanoscale cortex stiffness via condensation of cytoskeleton-focal adhesion plaque.Biophysical journal · 2025Article
- Pannexins in the musculoskeletal system: new targets for development and disease progression.Bone research · 2024Review
- [Role of Fibroblast Growth Factor 7 in Craniomaxillofacial Development].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2024Review
- The roles and regulatory mechanisms of TGF-β and BMP signaling in bone and cartilage development, homeostasis and disease.Cell research · 2024Review
- The Multifaceted Effects of Osteocytic TGFβ Signaling on the Skeletal and Extraskeletal Functions of Bone.Current osteoporosis reports · 2023Review
- Circulating macrophages as the mechanistic link between mosaic loss of Y-chromosome and cardiac disease.Cell & bioscience · 2023Article
- Contributions of Resin Cast Etching to Visualising the Osteocyte Lacuno-Canalicular Network Architecture in Bone Biology and Tissue Engineering.Calcified tissue international · 2023Review
- Subaqueous free-standing 3D cell culture system for ultrafast cell compaction, mechano-inductive immune control, and improving therapeutic angiogenesis.Bioengineering & translational medicine · 2023Article
- Accumulation of advanced oxidation protein products contributes to age-related impairment of gap junction intercellular communication in osteocytes of male mice.Bone & joint research · 2022Article
- Article
- Cx43 upregulation in HUVECs under stretch via TGF-β1 and cytoskeletal network.Open medicine (Warsaw, Poland) · 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
- FGF7-induced E11 facilitates cell-cell communication through connexin43.International journal of biological sciences · 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
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Connexins and pannexins are two families of channel forming proteins that are able to pass small molecules to achieve communication between cells. While connexins have been recognized to mediate gap junctional intercellular communication (GJIC), pannexins are far less known. Our previous study reported the potential role of TGF-β1 in mediating of connexins in osteocytes in vitro. Herein, we aimed to elucidate the influence of TGF-β1 on cell-cell communication based on gap junctions assembled by connexins and pannexins in vitro and ex vivo. We first showed that TGF-β1 positively affected the elongation of dendritic processes of osteocytes. Our data indicated that TGF-β1 increased expressions of connexin43 (Cx43) and pannexin1 (panx1), which are indispensable for hemichannel formation in gap junctions, in osteocytes in vitro and ex vivo. TGF-β1 enhanced gap junction formation and impacted cell-cell communication in living osteocytes, as indicated by the scrape loading and Lucifer yellow transfer assays. TGF-β1 enhanced the expressions of Cx43 and panx1 via activation of ERK1/2 and Smad3/4 signalling. The TGF-β1-restored expressions of Cx43 and panx1 in osteocytes in the presence of an ERK inhibitor, U0126, further demonstrated the direct participation of Smad3/4 signalling. TGF-β1 increased the accumulation of Smad3 in the nuclear region (immunofluorescence assay) and promoted the enrichment of Smad3 at the binding sites of the promoters of
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