ArticleInvestigative ophthalmology & visual science2011
Rapid changes in connexin-43 in response to genotoxic stress stabilize cell-cell communication in corneal endothelium.
Article in Investigative ophthalmology & visual science, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Dose- and Time-Dependent Modulation of Cx43 and Cx45 Expression and Gap Junction Conductance by Resveratrol.Antioxidants (Basel, Switzerland) · 2026Article
- PKCμ promotes keratinocyte cell migration through Cx43 phosphorylation-mediated suppression of intercellular communication.iScience · 2024Article
- Increased presynaptic excitability in a migraine with aura mutation.Brain : a journal of neurology · 2024Article
- Tumor Necrosis Factor-Alpha Disrupts Cx43-Mediated Corneal Endothelial Gap Junction Intercellular Communication.Oxidative medicine and cellular longevity · 2022Article
- Connexin30.3 is expressed in mouse embryonic stem cells and is responsive to leukemia inhibitory factor.Scientific reports · 2017Article
- Benzalkonium chloride suppresses rabbit corneal endothelium intercellular gap junction communication.PloS one · 2014Article
- The CK1 Family: Contribution to Cellular Stress Response and Its Role in Carcinogenesis.Frontiers in oncology · 2014Review
- Differentiation of human embryonic stem cells into cells with corneal keratocyte phenotype.PloS one · 2013Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
purposeTo determine how corneal endothelial (CE) cells respond to acute genotoxic stress through changes in connexin-43 (Cx43) and gap junction intercellular communication (GJIC).
methodsCultured bovine CE cells were exposed to mitomycin C or other DNA-damaging agents. Changes in the levels, stability, binding partners, and trafficking of Cx43 were assessed by Western blot analysis and immunostaining. Live-cell imaging of a Cx43-green fluorescent protein (GFP) fusion protein was used to evaluate internalization of cell surface Cx43. Dye transfer and fluorescent recovery after photobleaching (FRAP) assessed GJIC.
resultsAfter genotoxic stress, Cx43 accumulated in large gap junction plaques, had reduced zonula occludens-1 binding, and displayed increased stability. Live-cell imaging of Cx43-GFP plaques in stressed CE cells revealed reduced gap junction internalization and degradation compared to control cells. Mitomycin C enhanced transport of Cx43 from the endoplasmic reticulum to the cell surface and formation of gap junction plaques. Mitomycin C treatment also protected GJIC from disruption after cytokine treatment. DISCUSSION: These results show a novel CE cell response to genotoxic stress mediated by marked and rapid changes in Cx43 and GJIC. This stabilization of cell-cell communication may be an important early adaptation to acute stressors encountered by CE.
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Registered trials
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