Please use this identifier to cite or link to this item:
http://hdl.handle.net/1942/31181
Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Ramadan, Raghda | - |
dc.contributor.author | Vromans, Els | - |
dc.contributor.author | Anang, Dornatien Chuo | - |
dc.contributor.author | Goetschalckx, Ines | - |
dc.contributor.author | Hoorelbeke, Delphine | - |
dc.contributor.author | Decrock, Elke | - |
dc.contributor.author | Baatout, Sarah | - |
dc.contributor.author | LEYBAERT, Luc | - |
dc.contributor.author | Aerts, An | - |
dc.date.accessioned | 2020-05-21T15:00:21Z | - |
dc.date.available | 2020-05-21T15:00:21Z | - |
dc.date.issued | 2020 | - |
dc.date.submitted | 2020-05-19T11:38:54Z | - |
dc.identifier.citation | FRONTIERS IN PHARMACOLOGY, 11 (Art N° 212) | - |
dc.identifier.uri | http://hdl.handle.net/1942/31181 | - |
dc.description.abstract | Background Emerging evidence indicates an excess risk of late occurring cardiovascular diseases, especially atherosclerosis, after thoracic cancer radiotherapy. Ionizing radiation (IR) induces cellular effects which may induce endothelial cell dysfunction, an early marker for atherosclerosis. In addition, intercellular communication through channels composed of transmembrane connexin proteins (Cxs), i.e. Gap junctions (direct cell-cell coupling) and hemichannels (paracrine release/uptake pathway) can modulate radiation-induced responses and therefore the atherosclerotic process. However, the role of endothelial hemichannel in IR-induced atherosclerosis has never been described before. Materials and Methods Telomerase-immortalized human Coronary Artery/Microvascular Endothelial cells (TICAE/TIME) were exposed to X-rays (0.1 and 5 Gy). Production of reactive oxygen species (ROS), DNA damage, cell death, inflammatory responses, and senescence were assessed with or without applying a Cx43 hemichannel blocker (TAT-Gap19). Results We report here that IR induces an increase in oxidative stress, cell death, inflammatory responses (IL-8, IL-1 beta, VCAM-1, MCP-1, and Endothelin-1) and premature cellular senescence in TICAE and TIME cells. These effects are significantly reduced in the presence of the Cx43 hemichannel-targeting peptide TAT-Gap19. Conclusion Our findings suggest that endothelial Cx43 hemichannels contribute to various IR-induced processes, such as ROS, cell death, inflammation, and senescence, resulting in an increase in endothelial cell damage, which could be protected by blocking these hemichannels. Thus, targeting Cx43 hemichannels may potentially exert radioprotective effects. | - |
dc.description.sponsorship | RR is supported by a doctoral SCK center dot CEN/Ghent University Grant. | - |
dc.language.iso | en | - |
dc.publisher | FRONTIERS MEDIA SA | - |
dc.rights | 2020 Ramadan, Vromans, Anang, Goetschalckx, Hoorelbeke, Decrock, Baatout, Leybaert and Aerts. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. | - |
dc.subject.other | atherosclerosis | - |
dc.subject.other | endothelial damage | - |
dc.subject.other | ionizing radiation | - |
dc.subject.other | connexin43 hemichannels | - |
dc.subject.other | TAT-Gap19 | - |
dc.title | Connexin43 Hemichannel Targeting With TAT-Gap19 Alleviates Radiation-Induced Endothelial Cell Damage | - |
dc.type | Journal Contribution | - |
dc.identifier.volume | 11 | - |
local.format.pages | 19 | - |
local.bibliographicCitation.jcat | A1 | - |
dc.description.notes | Aerts, A (reprint author), Belgian Nucl Res Ctr SCK CEN, Radiobiol Unit, Mol, Belgium. | - |
dc.description.notes | an.aerts@sckcen.be | - |
local.publisher.place | AVENUE DU TRIBUNAL FEDERAL 34, LAUSANNE, CH-1015, SWITZERLAND | - |
local.type.refereed | Refereed | - |
local.type.specified | Article | - |
local.bibliographicCitation.artnr | 212 | - |
local.class | dsPublValOverrule/no_publishing_delay | - |
dc.source.type | Article | - |
dc.identifier.doi | 10.3389/fphar.2020.00212 | - |
dc.identifier.pmid | 32210810 | - |
dc.identifier.isi | WOS:000525480300001 | - |
dc.identifier.eissn | - | |
local.provider.type | wosris | - |
local.uhasselt.uhpub | yes | - |
local.uhasselt.international | no | - |
item.validation | ecoom 2021 | - |
item.fulltext | With Fulltext | - |
item.fullcitation | Ramadan, Raghda; Vromans, Els; Anang, Dornatien Chuo; Goetschalckx, Ines; Hoorelbeke, Delphine; Decrock, Elke; Baatout, Sarah; LEYBAERT, Luc & Aerts, An (2020) Connexin43 Hemichannel Targeting With TAT-Gap19 Alleviates Radiation-Induced Endothelial Cell Damage. In: FRONTIERS IN PHARMACOLOGY, 11 (Art N° 212). | - |
item.accessRights | Open Access | - |
item.contributor | Ramadan, Raghda | - |
item.contributor | Vromans, Els | - |
item.contributor | Anang, Dornatien Chuo | - |
item.contributor | Goetschalckx, Ines | - |
item.contributor | Hoorelbeke, Delphine | - |
item.contributor | Decrock, Elke | - |
item.contributor | Baatout, Sarah | - |
item.contributor | LEYBAERT, Luc | - |
item.contributor | Aerts, An | - |
crisitem.journal.issn | 1663-9812 | - |
crisitem.journal.eissn | 1663-9812 | - |
Appears in Collections: | Research publications |
Files in This Item:
File | Description | Size | Format | |
---|---|---|---|---|
fphar-11-00212.pdf | Published version | 7.68 MB | Adobe PDF | View/Open |
WEB OF SCIENCETM
Citations
31
checked on Jul 10, 2024
Page view(s)
40
checked on Sep 7, 2022
Download(s)
16
checked on Sep 7, 2022
Google ScholarTM
Check
Altmetric
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.