期刊
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
卷 70, 期 6, 页码 481-494出版社
OXFORD UNIV PRESS INC
DOI: 10.1097/NEN.0b013e31821db3aa
关键词
Blood brain barrier; Bone marrow chimeras; Claudin-5; Green fluorescence protein; Hippocampal formation; Major histocompatibility complex class I; Transient global cerebral ischemia
资金
- Danish MRC
- Lundbeck Foundation
- Leo Nielsen og Hustru Karen Margrethe Nielsens Fond
- Novo Nordic Foundation
- Aase and Ejnar Danielsen's Foundation
- Den Danske Laegeforening
- Else Poulsens Mindelegat
- Hede Nielsen Foundation
- Alice Brenaas Fond
- Fonden til Laegevidenskabens Fremme
- Faculty of Health Sciences, University of Southern Denmark
Current understanding of microglial involvement in disease is influenced by the observation that recruited bone marrow (BM)-derived cells contribute to reactive microgliosis in BM-chimeric mice. In contrast, a similar phenomenon has not been reported for BM-chimeric rats. We investigated the recruitment and microglial transformation of BM-derived cells in radiation BM-chimeric mice and rats after transient global cerebral ischemia, which elicits a characteristic microglial reaction. Both species displayed microglial hyperplasia and rod cell transformation in the hippocampal CA1 region. In mice, a sub-population of lesion-reactive microglia originated from transformed BM-derived cells. By contrast, no recruitment or microglial transformation of BM-derived cells was observed in BM-chimeric rats. These results suggest that reactive microglia in rats originate from resident microglia, whereas they have a mixed BM-derived and resident origin in mice, depending on the severity of ischemic tissue damage.
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