Radiotherapy of thoracic tumors increases the risk to develop cardiac diseases at later time-points. We compared time kinetics of radiation-induced changes of surface markers related to proliferation, progenitor cell development and inflammation in lung and heart microvascular endothelial cells (ECs).Mice received local thorax irradiation with a single dose of 0, 2 or 8Gy. Following magnetic bead separation and biotin-streptavidin competition, cell surface markers of isolated ECs from the lung and heart were analyzed 5, 10, 15 and 20weeks after irradiation by flow cytometry.Irradiation with 8Gy resulted in a temporary and differential up-regulation of proliferation markers (HCAM, Integrin ?-3, Endoglin, VE-cadherin, VEGFR-2) on ECs. Mucosialin a progenitor marker increased in lung ECs 15-20weeks and inflammatory markers (PECAM-1, ICAM-1, ICAM-2, VCAM-1) started to increase 10weeks after thorax irradiation with 8Gy. Interestingly, ICAM-1 and VCAM-1 remained up-regulated 20weeks after irradiation in heart and lung ECs.The persistently elevated expression density of ICAM-1 and VCAM-1 on ECs may suggest that an irradiation at 8Gy induces late inflammatory responses in heart and lung ECs.
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Radiotherapy of thoracic tumors increases the risk to develop cardiac diseases at later time-points. We compared time kinetics of radiation-induced changes of surface markers related to proliferation, progenitor cell development and inflammation in lung and heart microvascular endothelial cells (ECs).Mice received local thorax irradiation with a single dose of 0, 2 or 8Gy. Following magnetic bead separation and biotin-streptavidin competition, cell surface markers of isolated ECs from the lung a...
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