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Proteomic analysis by SILAC and 2D-DIGE reveals radiation-induced endothelial response: Four key pathways.

J. Proteomics 75, 2319-2330 (2012)
DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
Epidemiological data show that ionising radiation increases the risk of cardiovascular disease. The endothelium is one of the main targets of radiation-induced damage. Rapid radiation-induced alterations in the biological processes were investigated after exposure to a clinically relevant radiation dose (2.5Gy gamma radiation). The changes in protein expression were determined using the human endothelial cell line EA.hy926 as a model. Two complementary proteomic approaches, SILAC (Stable Isotope Labelling with Amino acids in Cell culture) and 2D-DIGE (Two Dimensional Difference-in-Gel-Electrophoresis) were used. The proteomes of the endothelial cells were analysed 4h and 24h after irradiation. Differentially expressed proteins were identified and quantified by MALDI-TOF/TOF and LTQ Orbitrap tandem mass spectrometry. The deregulated proteins were mainly categorised in four key pathways: (i) glycolysis/gluconeogenesis and synthesis/degradation of ketone bodies, (ii) oxidative phosphorylation, (iii) Rho-mediated cell motility and (iv) non-homologous end joining. We suggest that these alterations facilitate the repair processes needed to overcome the stress caused by irradiation and are indicative of the vascular damage leading to radiation-induced cardio- and cerebrovascular impairment.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter SILAC; 2D-DIGE; Ionising radiation; Cardiovascular diseases; Proteomics; Endothelial cells; CORONARY-HEART-DISEASE; MYOCARDIAL-INFARCTION; OXIDATIVE-PHOSPHORYLATION; QUANTITATIVE PROTEOMICS; PROTEIN QUANTIFICATION; IONIZING-RADIATION; BREAST-CANCER; CELL-CULTURE; AMINO-ACIDS; LONG-TERM
ISSN (print) / ISBN 1874-3919
e-ISSN 1876-7737
Zeitschrift Journal of Proteomics
Quellenangaben Band: 75, Heft: 8, Seiten: 2319-2330 Artikelnummer: , Supplement: ,
Verlag Elsevier
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed