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http://hdl.handle.net/1942/31170
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DC Field | Value | Language |
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dc.contributor.author | Baselet, Bjorn | - |
dc.contributor.author | DRIESEN, Ronald | - |
dc.contributor.author | Coninx, Emma | - |
dc.contributor.author | BELMANS, Niels | - |
dc.contributor.author | Sieprath, Tom | - |
dc.contributor.author | LAMBRICHTS, Ivo | - |
dc.contributor.author | De Vos, Winnok H. | - |
dc.contributor.author | Baatout, Sarah | - |
dc.contributor.author | Sonveaux, Pierre | - |
dc.contributor.author | Aerts, An | - |
dc.date.accessioned | 2020-05-21T09:37:57Z | - |
dc.date.available | 2020-05-21T09:37:57Z | - |
dc.date.issued | 2020 | - |
dc.date.submitted | 2020-05-19T13:24:53Z | - |
dc.identifier.citation | FRONTIERS IN PHARMACOLOGY, 11 (Art N° 268) | - |
dc.identifier.uri | http://hdl.handle.net/1942/31170 | - |
dc.description.abstract | Background and Purpose Up to 50-60% of all cancer patients receive radiotherapy as part of their treatment strategy. However, the mechanisms accounting for increased vascular risks after irradiation are not completely understood. Mitochondrial dysfunction has been identified as a potential cause of radiation-induced atherosclerosis. Materials and Methods Assays for apoptosis, cellular metabolism, mitochondrial DNA content, functionality and morphology were used to compare the response of endothelial cells to a single 2 Gy dose of X-rays under basal conditions or after pharmacological treatments that either reduced (EtBr) or increased (rosiglitazone) mitochondrial content. Results Exposure to ionizing radiation caused a persistent reduction in mitochondrial content of endothelial cells. Pharmacological reduction of mitochondrial DNA content rendered endothelial cells more vulnerable to radiation-induced apoptosis, whereas rosiglitazone treatment increased oxidative metabolism and redox state and decreased the levels of apoptosis after irradiation. Conclusion Pre-existing mitochondrial damage sensitizes endothelial cells to ionizing radiation-induced mitochondrial dysfunction. Rosiglitazone protects endothelial cells from the detrimental effects of radiation exposure on mitochondrial metabolism and oxidative stress. Thus, our findings indicate that rosiglitazone may have potential value as prophylactic for radiation-induced atherosclerosis. | - |
dc.description.sponsorship | This work was funded by EU FP7 DoReMi network of excellence (grant #249689), EU FP7 project ProCardio (grant #295823),the Belgian Federal Agency for Nuclear Control FANC-AFCN (grant #CO-90-13-3289-00) and the Belgian Fonds National de la Recherche Scientifique (F.R.S.-FNRS). BB, NB, and EC are supported by a doctoral SCK CEN grant. PS is a F.R.S.-FNRS Senior Research Associate. | - |
dc.language.iso | en | - |
dc.publisher | FRONTIERS MEDIA SA | - |
dc.rights | 2020 Baselet, Driesen, Coninx, Belmans, Sieprath, Lambrichts, De Vos, Baatout, Sonveaux 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 | ionizing radiation | - |
dc.subject.other | endothelial cells | - |
dc.subject.other | rosiglitazone | - |
dc.subject.other | mitochondria | - |
dc.subject.other | cardiovascular disease | - |
dc.title | Rosiglitazone Protects Endothelial Cells From Irradiation-Induced Mitochondrial Dysfunction | - |
dc.type | Journal Contribution | - |
dc.identifier.volume | 11 | - |
local.format.pages | 11 | - |
local.bibliographicCitation.jcat | A1 | - |
dc.description.notes | Aerts, A (reprint author), Belgian Nucl Res Ctr SCK CEN, Inst Environm Hlth & Safety, Radiobiol Unit, Mol, Belgium. | - |
dc.description.notes | an.aerts@sckcen.be | - |
dc.description.other | Aerts, A (reprint author), Belgian Nucl Res Ctr SCK CEN, Inst Environm Hlth & Safety, Radiobiol Unit, Mol, Belgium. 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 | 268 | - |
dc.source.type | Article | - |
dc.identifier.doi | 10.3389/fphar.2020.00268 | - |
dc.identifier.pmid | 32231569 | - |
dc.identifier.isi | WOS:000525604600001 | - |
dc.contributor.orcid | Lambrichts, Ivo/0000-0001-7520-0021 | - |
dc.identifier.eissn | - | |
local.provider.type | wosris | - |
local.uhasselt.uhpub | yes | - |
local.uhasselt.international | no | - |
item.contributor | Baselet, Bjorn | - |
item.contributor | DRIESEN, Ronald | - |
item.contributor | Coninx, Emma | - |
item.contributor | BELMANS, Niels | - |
item.contributor | Sieprath, Tom | - |
item.contributor | LAMBRICHTS, Ivo | - |
item.contributor | De Vos, Winnok H. | - |
item.contributor | Baatout, Sarah | - |
item.contributor | Sonveaux, Pierre | - |
item.contributor | Aerts, An | - |
item.validation | ecoom 2021 | - |
item.fullcitation | Baselet, Bjorn; DRIESEN, Ronald; Coninx, Emma; BELMANS, Niels; Sieprath, Tom; LAMBRICHTS, Ivo; De Vos, Winnok H.; Baatout, Sarah; Sonveaux, Pierre & Aerts, An (2020) Rosiglitazone Protects Endothelial Cells From Irradiation-Induced Mitochondrial Dysfunction. In: FRONTIERS IN PHARMACOLOGY, 11 (Art N° 268). | - |
item.accessRights | Open Access | - |
item.fulltext | With Fulltext | - |
crisitem.journal.eissn | 1663-9812 | - |
Appears in Collections: | Research publications |
Files in This Item:
File | Description | Size | Format | |
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fphar-11-00268 (1).pdf | Published version | 4.53 MB | Adobe PDF | View/Open |
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