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A role for endothelial cells in radiation-induced inflammation

Artikel i vetenskaplig tidskrift
Författare Martina Boström
Marie Kalm
Yohanna Eriksson
Cecilia Bull
Anders Ståhlberg
Thomas Björk-Eriksson
Nina Hellström Erkenstam
Klas Blomgren
Publicerad i International Journal of Radiation Biology
Volym 94
Nummer/häfte 3
Sidor 259-271
ISSN 0955-3002
Publiceringsår 2018
Publicerad vid Institutionen för neurovetenskap och fysiologi
Institutionen för kliniska vetenskaper, Avdelningen för onkologi
Institutionen för biomedicin, avdelningen för patologi
Sahlgrenska Cancer Center
Institutionen för neurovetenskap och fysiologi, sektionen för farmakologi
Sidor 259-271
Språk en
Länkar https://doi.org/10.1080/09553002.20...
Ämnesord Hippocampus, cerebellum, neuroinflammation, radiotherapy, developing brain, eotaxin, childhood cns malignancies, aging systemic milieu, young-mouse brain, hippocampal neurogenesis, ionizing-radiation, cognitive function, long-term, neurocognitive sequelae, tumor response, irradiation, Life Sciences & Biomedicine - Other Topics, Nuclear Science &, Technology, Radiology, Nuclear Medicine & Medical Imaging
Ämneskategorier Radiologi, Strålningsbiologi, Radiologi och bildbehandling

Sammanfattning

Purpose: To unravel the role of the vasculature in radiation-induced brain tissue damage.Materials and methods: Postnatal day 14 mice received a single dose of 10Gy cranial irradiation and were sacrificed 6h, 24h or 7 days post-irradiation. Endothelial cells were isolated from the hippocampus and cerebellum using fluorescence-activated cell sorting, followed by cell cycle analysis and gene expression profiling.Results: Flow cytometric analysis revealed that irradiation increased the percentage of endothelial cells, relative to the whole cell population in both the hippocampus and the cerebellum. This change in cell distribution indicates that other cell types are more susceptible to irradiation-induced cell death, compared to endothelial cells. This was supported by data showing that genes involved in endothelial cell-specific apoptosis (e.g. Smpd1) were not induced at any time point investigated but that genes involved in cell-cycle arrest (e.g. Cdkn1a) were upregulated at all investigated time points, indicating endothelial cell repair. Inflammation-related genes, on the other hand, were strongly induced, such as Ccl2, Ccl11 and Il6.Conclusions: We conclude that endothelial cells are relatively resistant to ionizing radiation but that they play an active, hitherto unknown, role in the inflammatory response after irradiation. In the current study, this was shown in both the hippocampus, where neurogenesis and extensive cell death after irradiation occurs, and in the cerebellum, where neurogenesis no longer occurs at this developmental age.

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