2014
DOI: 10.1136/heartjnl-2014-306916.21
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UNDERSTANDING THE EFFECTS OF CANCER RADIATION THERAPY ON ENDOTHELIAL CELL DYSFUNCTION – THE ROLE OF NFκB/JNK

Abstract: Cardiovascular disease is the principal cause of mortality in developed societies. Studies have identified a correlation between radiotherapy for cancer and atherosclerosis in later life1. Endothelial cell dysfunction is a defining feature of atherosclerosis initiation. This study aims to investigate the effect of radiation on endothelial cell intracellular signalling networks, including the Nuclear Factor-kappaB (NFκB) and c-Jun N-terminal kinase (JNK) pathways. Human umbilical vein endothelial cells (HUVECs)… Show more

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“…Radiation stimulates the formation of ceramide, thereby reducing the stability of the mitochondrial membrane and promoting apoptosis through the JNK pathway. 25,26 JNK can be activated by various stimuli, controls the intracellular and extracellular stress reactions of cells, which is called the stress-activated protein kinase (SAPK), and it plays a very important role in regulating cell apoptosis. 39,40 In the present study, irradiation increased the p-JNK and cleaved caspase-3 expression in HBMECs, while celecoxib partially reversed these increases.…”
Section: Discussionmentioning
confidence: 99%
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“…Radiation stimulates the formation of ceramide, thereby reducing the stability of the mitochondrial membrane and promoting apoptosis through the JNK pathway. 25,26 JNK can be activated by various stimuli, controls the intracellular and extracellular stress reactions of cells, which is called the stress-activated protein kinase (SAPK), and it plays a very important role in regulating cell apoptosis. 39,40 In the present study, irradiation increased the p-JNK and cleaved caspase-3 expression in HBMECs, while celecoxib partially reversed these increases.…”
Section: Discussionmentioning
confidence: 99%
“…On the other hand, radiation can stimulate the formation of ceramide, thereby reducing the stability of the mitochondrial membrane and promoting apoptosis through the c-Jun N-terminal kinase (JNK) pathway. 25,26 JNK can be activated by a variety of stimuli, such as oxidative damage, DNA and endoplasmic reticulum damage. 27 The activated form of JNK is phosphorylated JNK (p-JNK), which translocates to the cytoplasm, activating caspase-3 and the mitochondrial apoptotic pathway.…”
Section: Introductionmentioning
confidence: 99%
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