Wolfgang Sievert1, Klaus-Rüdiger Trott2, Omid Azimzadeh3, Soile Tapio3, Horst Zitzelsberger4, Gabriele Multhoff5. 1. Department of Radiation Oncology, Technische Universität München, Helmholtz Zentrum München (HMGU), German Research Center for Environmental Health Munich, Neuherberg, Germany. 2. Department of Oncology, Imperial University College London, UK. 3. Institute of Radiation Biology, Helmholtz Zentrum München (HMGU), German Research Center for Environmental Health Munich, Neuherberg, Germany. 4. Research Unit Radiation Cytogenetics, Helmholtz Zentrum München (HMGU), German Research Center for Environmental Health Munich, Neuherberg, Germany. 5. Department of Radiation Oncology, Technische Universität München, Helmholtz Zentrum München (HMGU), German Research Center for Environmental Health Munich, Neuherberg, Germany. Electronic address: gabriele.multhoff@lrz.tu-muenchen.de.
Abstract
BACKGROUND AND PURPOSE: 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). MATERIAL AND METHODS: Mice received local thorax irradiation with a single dose of 0, 2 or 8 Gy. 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 20 weeks after irradiation by flow cytometry. RESULTS: Irradiation with 8 Gy resulted in a temporary and differential up-regulation of proliferation markers (HCAM, Integrin β-3, Endoglin, VE-cadherin, VEGFR-2) on ECs. Mucosialin a progenitor marker increased in lung ECs 15-20 weeks and inflammatory markers (PECAM-1, ICAM-1, ICAM-2, VCAM-1) started to increase 10 weeks after thorax irradiation with 8 Gy. Interestingly, ICAM-1 and VCAM-1 remained up-regulated 20 weeks after irradiation in heart and lung ECs. CONCLUSIONS: The persistently elevated expression density of ICAM-1 and VCAM-1 on ECs may suggest that an irradiation at 8 Gy induces late inflammatory responses in heart and lung ECs.
BACKGROUND AND PURPOSE: 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). MATERIAL AND METHODS:Mice received local thorax irradiation with a single dose of 0, 2 or 8 Gy. 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 20 weeks after irradiation by flow cytometry. RESULTS: Irradiation with 8 Gy resulted in a temporary and differential up-regulation of proliferation markers (HCAM, Integrin β-3, Endoglin, VE-cadherin, VEGFR-2) on ECs. Mucosialin a progenitor marker increased in lung ECs 15-20 weeks and inflammatory markers (PECAM-1, ICAM-1, ICAM-2, VCAM-1) started to increase 10 weeks after thorax irradiation with 8 Gy. Interestingly, ICAM-1 and VCAM-1 remained up-regulated 20 weeks after irradiation in heart and lung ECs. CONCLUSIONS: The persistently elevated expression density of ICAM-1 and VCAM-1 on ECs may suggest that an irradiation at 8 Gy induces late inflammatory responses in heart and lung ECs.
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