Rosiglitazone protects endothelial cells from irradiation-induced mitochondiral dysfunction

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Rosiglitazone protects endothelial cells from irradiation-induced mitochondiral dysfunction. / Baselet, Bjorn; Driesen, Ronald B.; Coninx, Emma; Belmans, Niels; Sieprath, Tom; Lambrichts, Ivo; De Vos, Winnok H.; Baatout, Sarah; Sonveaux, Pierre; Aerts, An.

In: Frontiers in Pharmacology, Vol. March, No. 2020, 13.03.2020, p. 1-11.

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Baselet, B, Driesen, RB, Coninx, E, Belmans, N, Sieprath, T, Lambrichts, I, De Vos, WH, Baatout, S, Sonveaux, P & Aerts, A 2020, 'Rosiglitazone protects endothelial cells from irradiation-induced mitochondiral dysfunction', Frontiers in Pharmacology, vol. March, no. 2020, pp. 1-11. https://doi.org/10.3389/fphar.2020.00268

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Baselet, Bjorn ; Driesen, Ronald B. ; Coninx, Emma ; Belmans, Niels ; Sieprath, Tom ; Lambrichts, Ivo ; De Vos, Winnok H. ; Baatout, Sarah ; Sonveaux, Pierre ; Aerts, An. / Rosiglitazone protects endothelial cells from irradiation-induced mitochondiral dysfunction. In: Frontiers in Pharmacology. 2020 ; Vol. March, No. 2020. pp. 1-11.

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@article{678c12c796d74008be97dda8e50ebc8d,
title = "Rosiglitazone protects endothelial cells from irradiation-induced mitochondiral dysfunction",
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.",
keywords = "Ionizing radiation, Endothelial cells, Rosiglitazone, Mitochondria, Cardiovascular disease",
author = "Bjorn Baselet and Driesen, {Ronald B.} and Emma Coninx and Niels Belmans and Tom Sieprath and Ivo Lambrichts and {De Vos}, {Winnok H.} and Sarah Baatout and Pierre Sonveaux and An Aerts",
note = "Score=10",
year = "2020",
month = "3",
day = "13",
doi = "10.3389/fphar.2020.00268",
language = "English",
volume = "March",
pages = "1--11",
journal = "Frontiers in Pharmacology",
issn = "1663-9812",
publisher = "Frontiers Media",
number = "2020",

}

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TY - JOUR

T1 - Rosiglitazone protects endothelial cells from irradiation-induced mitochondiral dysfunction

AU - Baselet, Bjorn

AU - Driesen, Ronald B.

AU - Coninx, Emma

AU - Belmans, Niels

AU - Sieprath, Tom

AU - Lambrichts, Ivo

AU - De Vos, Winnok H.

AU - Baatout, Sarah

AU - Sonveaux, Pierre

AU - Aerts, An

N1 - Score=10

PY - 2020/3/13

Y1 - 2020/3/13

N2 - 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.

AB - 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.

KW - Ionizing radiation

KW - Endothelial cells

KW - Rosiglitazone

KW - Mitochondria

KW - Cardiovascular disease

UR - https://ecm.sckcen.be/OTCS/llisapi.dll/open/37730838

U2 - 10.3389/fphar.2020.00268

DO - 10.3389/fphar.2020.00268

M3 - Article

VL - March

SP - 1

EP - 11

JO - Frontiers in Pharmacology

JF - Frontiers in Pharmacology

SN - 1663-9812

IS - 2020

ER -

ID: 6758185