Pathological effects of ionizing radiation: endothelial activation and dysfunction

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Abstract

The endothelium, a tissue that forms a single layer of cells lining various organs and cavities of the body, especially the heart and blood as well as lymphatic vessels, plays a complex role in vascular biology. It contributes to key aspects of vascular homeostasis and is also involved in pathophysiological processes, such as thrombosis, inflammation, and hypertension. Epidemiological data show that high doses of ionizing radiation lead to cardiovascular disease over time. The aim of this review is to summarize the current knowledge on endothelial cell activation and dysfunction after ionizing radiation exposure as a central feature preceding the development of cardiovascular diseases.

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Cytochrome c and dATP-dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascade.

P. Li, D Nijhawan, I Budihardjo … (1997)

We report here the purification of the third protein factor, Apaf-3, that participates in caspase-3 activation in vitro. Apaf-3 was identified as a member of the caspase family, caspase-9. Caspase-9 and Apaf-1 bind to each other via their respective NH2-terminal CED-3 homologous domains in the presence of cytochrome c and dATP, an event that leads to caspase-9 activation. Activated caspase-9 in turn cleaves and activates caspase-3. Depletion of caspase-9 from S-100 extracts diminished caspase-3 activation. Mutation of the active site of caspase-9 attenuated the activation of caspase-3 and cellular apoptotic response in vivo, indicating that caspase-9 is the most upstream member of the apoptotic protease cascade that is triggered by cytochrome c and dATP.

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Apaf-1, a human protein homologous to C. elegans CED-4, participates in cytochrome c-dependent activation of caspase-3.

Hua Zou, William Henzel, Xuesong Liu … (1997)

We report here the purification and cDNA cloning of Apaf-1, a novel 130 kd protein from HeLa cell cytosol that participates in the cytochrome c-dependent activation of caspase-3. The NH2-terminal 85 amino acids of Apaf-1 show 21% identity and 53% similarity to the NH2-terminal prodomain of the Caenorhabditis elegans caspase, CED-3. This is followed by 320 amino acids that show 22% identity and 48% similarity to CED-4, a protein that is believed to initiate apoptosis in C. elegans. The COOH-terminal region of Apaf-1 comprises multiple WD repeats, which are proposed to mediate protein-protein interactions. Cytochrome c binds to Apaf-1, an event that may trigger the activation of caspase-3, leading to apoptosis.

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Long-term follow-up of patients with mild coronary artery disease and endothelial dysfunction.

J Suwaidi, S Hamasaki, S T Higano … (2000)

Coronary endothelial dysfunction is characterized by vasoconstrictive response to the endothelium-dependent vasodilator acetylcholine. Although endothelial dysfunction is considered an early phase of coronary atherosclerosis, there is a paucity of information regarding the outcome of these patients. Thus, this study was designed to evaluate the outcome of patients with mild coronary artery disease on the basis of their endothelial function. Follow-up was obtained in 157 patients with mildly diseased coronary arteries who had undergone coronary vascular reactivity evaluation by graded administration of intracoronary acetylcholine, adenosine, and nitroglycerin and intracoronary ultrasound at the time of diagnostic study. Patients were divided on the basis of their response to acetylcholine into 3 groups: group 1 (n=83), patients with normal endothelial function; group 2 (n=32), patients with mild endothelial dysfunction; and group 3 (n=42), patients with severe endothelial dysfunction. Over an average 28-month follow-up (range, 11 to 52 months), none of the patients from group 1 or 2 had cardiac events. However, 6 (14%) with severe endothelial dysfunction had 10 cardiac events (P<0.05 versus groups 1 and 2). Cardiac events included myocardial infarction, percutaneous or surgical coronary revascularization, and/or cardiac death. Severe endothelial dysfunction in the absence of obstructive coronary artery disease is associated with increased cardiac events. This study supports the concept that coronary endothelial dysfunction may play a role in the progression of coronary atherosclerosis.

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Author and article information

Contributors

An Aerts: +32 (0) 14 33 23 90 , an.aerts@sckcen.be

Journal

Journal ID (nlm-ta): Cell Mol Life Sci

Journal ID (iso-abbrev): Cell. Mol. Life Sci

Title: Cellular and Molecular Life Sciences

Publisher: Springer International Publishing (Cham )

ISSN (Print): 1420-682X

ISSN (Electronic): 1420-9071

Publication date (Electronic): 30 October 2018

Publication date PMC-release: 30 October 2018

Publication date (Print): 2019

Volume: 76

Issue: 4

Pages: 699-728

Affiliations

[1 ]ISNI 0000 0000 9332 3503, GRID grid.8953.7, Radiobiology Unit, , Belgian Nuclear Research Centre (SCK•CEN), ; Mol, Belgium

[2 ]ISNI 0000 0001 2294 713X, GRID grid.7942.8, Institute of Experimental and Clinical Research (IREC), Pole of Pharmacology and Therapeutics, , Université catholique de Louvain (UCL), ; Brussels, Belgium

[3 ]ISNI 0000 0001 2069 7798, GRID grid.5342.0, Department of Molecular Biotechnology, , Ghent University, ; Ghent, Belgium

Article

Publisher ID: 2956

DOI: 10.1007/s00018-018-2956-z

PMC ID: 6514067

PubMed ID: 30377700

SO-VID: e2fcf41f-b675-4c54-b3a8-0578a7844ec7

License:

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

History

Date received : 11 May 2018

Date revision received : 19 October 2018

Date accepted : 23 October 2018

Funding

Funded by: FP7 DoReMi

Award ID: 249689

Funded by: FP7 ProCardio

Award ID: 295823

Funded by: Federal agency for nuclear control

Award ID: CO-90-13-3289-00

Funded by: FundRef http://dx.doi.org/10.13039/501100002661, Fonds De La Recherche Scientifique - FNRS;

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ScienceOpen disciplines: Molecular biology

Keywords: vascular tone,procoagulation,prothrombosis,endothelial cell retraction,mitochondrial dysfunction,premature senescence

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ScienceOpen disciplines: Molecular biology

Keywords: vascular tone, procoagulation, prothrombosis, endothelial cell retraction, mitochondrial dysfunction, premature senescence

Pathological effects of ionizing radiation: endothelial activation and dysfunction

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Abstract

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Most cited references 220

Cytochrome c and dATP-dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascade.

Apaf-1, a human protein homologous to C. elegans CED-4, participates in cytochrome c-dependent activation of caspase-3.

Long-term follow-up of patients with mild coronary artery disease and endothelial dysfunction.

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