期刊
ACTA NEUROPATHOLOGICA
卷 120, 期 2, 页码 223-236出版社
SPRINGER
DOI: 10.1007/s00401-010-0704-z
关键词
Brain inflammation; Multiple sclerosis; Astrocytes; Demyelination; Neuromyelitis optica
资金
- Communication in Health and Disease (CCHD)
- Medical University Vienna
- Austrian Science Fund (FWF) [P19854-B02, P21581-B09]
- European Union [LSHM-CT-2005-018637]
- UK MRC
- Multiple Sclerosis Society
- Brain Research Trust
- MRC [G0800954, G0500814] Funding Source: UKRI
- Austrian Science Fund (FWF) [P21581] Funding Source: Austrian Science Fund (FWF)
- Austrian Science Fund (FWF) [P 21581] Funding Source: researchfish
- Medical Research Council [G0500814, G0800954] Funding Source: researchfish
Primary loss and dysfunction of astrocytes may trigger demyelination, as seen in neuromyelitis optica, an inflammatory disease of the central nervous system. In most patients affected by this disease, injury to astrocytes is initiated by the action of autoantibodies targeting aquaporin 4 (AQP-4), a water channel on astrocytes. We show here that damage of astrocytes and subsequent demyelination can also occur in the absence of autoantibody-mediated mechanisms. Following injection of lipopolysaccharide into the white matter initial microglia activation is followed by a functional disturbance of astrocytes, mainly reflected by retraction of astrocytic foot processes at the glia limitans and loss of AQP-4 and connexins, which are involved in the formation of gap junctions between astrocytes and oligodendrocytes. Demyelination and oligodendrocyte degeneration in this model follows astrocyte pathology. Similar structural abnormalities were also seen in a subset of active lesions in multiple sclerosis. Our studies suggest that astrocyte injury may be an important early step in the cascade of lesion formation in brain inflammation.
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