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Pluder, F. ; Barjaktarovic, Z. ; Azimzadeh, O. ; Mörtl, S. ; Krämer, A. ; Steininger, S. ; Sarioglu, H. ; Leszczynski, D.* ; Nylund, R.* ; Hakanen, A.* ; Sriharshan, A. ; Atkinson, M.J. ; Tapio, S.

Low-dose irradiation causes rapid alterations to the proteome of the human endothelial cell line EA.hy926.

Radiat. Environ. Biophys. 50, 155-166 (2011)
DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
High doses of ionising radiation damage the heart by an as yet unknown mechanism. A concern for radiological protection is the recent epidemiological data indicating that doses as low as 100-500 mGy may induce cardiac damage. The aim of this study was to identify potential molecular targets and/or mechanisms involved in the pathogenesis of low-dose radiation-induced cardiovascular disease. The vascular endothelium plays a pivotal role in the regulation of cardiac function and is therefore a potential target tissue. We report here that low-dose radiation induced rapid and time-dependent changes in the cytoplasmic proteome of the human endothelial cell line EA.hy926. The proteomes were investigated at 4 and 24 h after irradiation at two different dose rates (Co-60 gamma ray total dose 200 mGy; 20 mGy/min and 190 mGy/min) using 2D-DIGE technology. Differentially expressed proteins were identified, after in-gel trypsin digestion, by MALDI-TOF/TOF tandem mass spectrometry, and peptide mass fingerprint analyses. We identified 15 significantly differentially expressed proteins, of which 10 were up-regulated and 5 down-regulated, with more than ± 1.5-fold difference compared with unexposed cells. Pathways influenced by the low-dose exposures included the Ran and RhoA pathways, fatty acid metabolism and stress response.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Ionising radiation; proteomics; low dose; endothelial; radiation-induced cardiovascular disease; reactive oxygen species; dose rate
ISSN (print) / ISBN 0301-634X
e-ISSN 1432-2099
Quellenangaben Band: 50, Heft: 1, Seiten: 155-166 Artikelnummer: , Supplement: ,
Verlag Springer
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed