Influence of irradiation on release of endothelial microparticles (EMP) in vitro
Issue title: Selected Presentations held at the 34th Conference of the German Society for Clinical Microcirculation and Hemorheology, Regensburg, Germany, 27–28 November, 2015
Affiliations: [a] Helmholtz-Zentrum Dresden-Rossendorf, Institute of Radiopharmaceutical Cancer Research, Department of Radiopharmaceutical and Chemical Biology, Dresden, Germany | [b] Technische Universität Dresden, Department of Chemistry and Food Chemistry, Dresden, Germany
Correspondence:
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Corresponding author: Jens Pietzsch, PhD, MD, Helmholtz-Zentrum Dresden-Rossendorf, Institute of Radiopharmaceutical Cancer Research, Department of Radiopharmaceutical and Chemical Biology, Bautzner Landstrasse 400, 01328 Dresden, Germany. Tel.: +49 3512602622; Fax: +49 35126012622; E-mail: j.pietzsch@hzdr.de
Abstract: Survivors of Hodgkin’s disease as well as of breast and lung cancer are at risk of radiation-associated cardiovascular disease. Recent studies demonstrated a correlation between cardiovascular risk factors and circulating endothelial microparticles (EMP) and thereby suggest increased EMP levels in circulation to be an early biomarker of endothelial dysfunction and cardiovascular risk. This prompted us to analyze the amount of EMP released by human aortic endothelial cells (HAEC) after exposure to different doses of X-ray (0.4, 2, 4, 6, and 20 Gy) using antibodies against the endothelial cell markers CD31, CD144, and CD146 by flow cytometry. In this pilot experiment only CD146 proved appropriate for quantification of HAEC-derived EMP. Exposure of HAEC to different doses of X-ray did not significantly influence formation of CD146-positive EMP. However, low doses (0.4 Gy) tended to decrease EMP formation, whereas higher doses (2 or 4 Gy) slightly increased release of CD146-positive EMP. By contrast, inflammatory activation of HAEC by TPA significantly increased EMP release about 15-fold (P < 0.01). In conclusion, under the present experimental conditions EMP did not prove a suitable biomarker for radiation-induced endothelial dysfunction in vitro.
