ArticleThe American journal of pathology2013
Human articular chondrocytes express multiple gap junction proteins: differential expression of connexins in normal and osteoarthritic cartilage.
Article in The American journal of pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 72 citations in OpenAlex.
- Participation of the purinergic P2X7 receptor in molecular complexes in the nucleus of human chondrocytes.Cellular and molecular life sciences : CMLS · 2026Article
- Loss of connexin 43 in cartilage causes mitochondrial dysfunction and accelerates post-traumatic osteoarthritis progression.bioRxiv : the preprint server for biology · 2026Article
- Targeting mechanotransduction components as therapeutic strategies in osteoarthritis.Molecular biology reports · 2026Review
- Chondrocyte Senescence in Osteoarthritis: Potential Targets and Pharmacological Interventions.Cartilage · 2026Article
- Multiple strategies, one mission: mesenchymal stromal cell-based mechanisms of action in osteoarthritis.Frontiers in cell and developmental biology · 2026Review
- Identification of Genes Linked to Meniscal Degeneration in Osteoarthritis: An In Silico Analysis.International journal of molecular sciences · 2025Article
- Connexin 43 regulates intercellular mitochondrial transfer from human mesenchymal stromal cells to chondrocytes.Stem cell research & therapy · 2024Article
- Connexin 43 Modulation in Human Chondrocytes, Osteoblasts and Cartilage Explants: Implications for Inflammatory Joint Disorders.International journal of molecular sciences · 2024Article
- "Genetic scissors" CRISPR/Cas9 genome editing cutting-edge biocarrier technology for bone and cartilage repair.Bioactive materials · 2023Review
- Timing Expression of miR203a-3p during OA Disease: Preliminary In Vitro Evidence.International journal of molecular sciences · 2023Article
- Functional Roles of Connexins and Gap Junctions in Osteo-Chondral Cellular Components.International journal of molecular sciences · 2023Review
- The roles of connexins and gap junctions in the progression of cancer.Cell communication and signaling : CCS · 2023Review
- Mesenchymal stromal cells donate mitochondria to articular chondrocytes exposed to mitochondrial, environmental, and mechanical stress.Scientific reports · 2022Article
- Connexin43 in Musculoskeletal System: New Targets for Development and Disease Progression.Aging and disease · 2022Article
- Structural clues to articular calcified cartilage function: A descriptive review of this crucial interface tissue.Journal of anatomy · 2022Review
- Potential Methods of Targeting Cellular Aging Hallmarks to Reverse Osteoarthritic Phenotype of Chondrocytes.Biology · 2022Review
- Dynamics of Connexin 43 Down Modulation in Human Articular Chondrocytes Stimulated by Tumor Necrosis Factor Alpha.International journal of molecular sciences · 2022Article
- Osteoarthritis: Mechanistic Insights, Senescence, and Novel Therapeutic Opportunities.Bioelectricity · 2022Article
- ATP transporters in the joints.Purinergic signalling · 2021Review
- Ex Vivo Generation and Characterization of Human Hyaline and Elastic Cartilaginous Microtissues for Tissue Engineering Applications.Biomedicines · 2021Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Osteoarthritis (OA) is the most common joint disease and involves progressive degeneration of articular cartilage. The aim of this study was to investigate if chondrocytes from human articular cartilage express gap junction proteins called connexins (Cxs). We show that human chondrocytes in tissue express Cx43, Cx45, Cx32, and Cx46. We also find that primary chondrocytes from adults retain the capacity to form functional voltage-dependent gap junctions. Immunohistochemistry experiments in cartilage from OA patients revealed significantly elevated levels of Cx43 and Cx45 in the superficial zone and down through the next approximately 1000 μm of tissue. These zones corresponded with regions damaged in OA that also had high levels of proliferative cell nuclear antigen. An increased number of Cxs may help explain the increased proliferation of cells in clusters that finally lead to tissue homeostasis loss. Conversely, high levels of Cxs in OA cartilage reflect the increased number of adjacent cells in clusters that are able to interact directly by gap junctions as compared with hemichannels on single cells in normal cartilage. Our data provide strong evidence that OA patients have a loss of the usual ordered distribution of Cxs in the damaged zones and that the reductions in Cx43 levels are accompanied by the loss of correct Cx localization in the nondamaged areas.
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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.