ArticleScientific reports2019
Single and fractionated ionizing radiation induce alterations in endothelial connexin expression and channel function.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- Radiation meets inflammation: NLRP3 inflammasome at the core of radiation-induced cardiac injury.Journal of translational medicine · 2025Review
- Review
- The role of cell junctions in atherosclerosis: implications for inflammation, endothelial dysfunction, and plaque stability.Journal of physiology and biochemistry · 2025Review
- Intersection of Cardio-Oncology: An Overview of Radiation-Induced Heart Disease in the Context of Tumors.Journal of the American Heart Association · 2025Review
- A Case of Filter Retrieval With an Aspiration Catheter for Filter Occlusion in Emergency Carotid Artery Stenting.Cureus · 2024Article
- The Potential Role of Connexins in the Pathogenesis of Atherosclerosis.International journal of molecular sciences · 2023Review
- DNA Methylation Alterations in Fractionally Irradiated Rats and Breast Cancer Patients Receiving Radiotherapy.International journal of molecular sciences · 2022Article
- Article
- X‑irradiation induces acute and early term inflammatory responses in atherosclerosis‑prone ApoE‑/‑ mice and in endothelial cells.Molecular medicine reports · 2021Article
- The role of connexin proteins and their channels in radiation-induced atherosclerosis.Cellular and molecular life sciences : CMLS · 2021Review
- Review of Stereotactic Arrhythmia Radioablation Therapy for Cardiac Tachydysrhythmias.CJC open · 2021Review
- Radiation-Induced Salivary Gland Dysfunction: Mechanisms, Therapeutics and Future Directions.Journal of clinical medicine · 2020Review
- Dexmedetomidine Attenuates Monocyte-Endothelial Adherence via Inhibiting Connexin43 on Vascular Endothelial Cells.Mediators of inflammation · 2020Article
- Connexin43 Hemichannel Targeting With TAT-Gap19 Alleviates Radiation-Induced Endothelial Cell Damage.Frontiers in pharmacology · 2020Article
- The Role of NLRP3 Inflammasome in Radiation-Induced Cardiovascular Injury.Frontiers in cell and developmental biology · 2020Review
- Inverse dose protraction effects of low-LET radiation: Evidence and significance.Mutation research. Reviews in mutation researchReview
- Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Radiotherapy is an effective treatment for most tumor types. However, emerging evidence indicates an increased risk for atherosclerosis after ionizing radiation exposure, initiated by endothelial cell dysfunction. Interestingly, endothelial cells express connexin (Cx) proteins that are reported to exert proatherogenic as well as atheroprotective effects. Furthermore, Cxs form channels, gap junctions and hemichannels, that are involved in bystander signaling that leads to indirect radiation effects in non-exposed cells. We here aimed to investigate the consequences of endothelial cell irradiation on Cx expression and channel function. Telomerase immortalized human Coronary Artery/Microvascular Endothelial cells were exposed to single and fractionated X-rays. Several biological endpoints were investigated at different time points after exposure: Cx gene and protein expression, gap junctional dye coupling and hemichannel function. We demonstrate that single and fractionated irradiation induce upregulation of proatherogenic Cx43 and downregulation of atheroprotective Cx40 gene and protein levels in a dose-dependent manner. Single and fractionated irradiation furthermore increased gap junctional communication and induced hemichannel opening. Our findings indicate alterations in Cx expression that are typically observed in endothelial cells covering atherosclerotic plaques. The observed radiation-induced increase in Cx channel function may promote bystander signaling thereby exacerbating endothelial cell damage and atherogenesis.
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