期刊
EXPERIMENTAL NEUROLOGY
卷 201, 期 2, 页码 349-358出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.expneurol.2006.04.030
关键词
EAE; multiple sclerosis; demyelination; gliosis; Olig2; NG2; Nkx2.2
资金
- Intramural NIH HHS Funding Source: Medline
The injury response in the brain involves complex interplay between neural and immune components. Following inflammatory insults to the adult CNS. formation of an astroglial scar often impedes functional repair. Glial progenitor cells expressing the nuclear transcription factor Olig2 possibly generate astrocytes in response to various types of injuries; however, the mechanisms underlying this differentiation are unclear. In a model of immune-mediated injury (MOG(35-55)-experimental autoimmune encephalomyelitis), we show that the conversion from progenitor to reactive astrocyte is marked by the translocation of Olig2 into the cytoplasm. Evidence of this process is found for months after disease initiation in the absence of new inflammatory infiltrates. A proportion of cells with cytoplasmic Olig2 was found to express NG2 or Nkx2.2, but only Nkx2.2 was occasionally retained by GFAP(+) cells. We further show that differentiation to astrocytes is induced in glial progenitors in vitro through exposure to the pro-inflammatory cytokine IFN-gamma, but not to TNF-alpha. Together, these data ascribe a pivotal role to Olig2(+) glial precursor cells in the adult GINS. linking autoimmune inflammation and glial scar formation. (c) 2006 Elsevier Inc. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据