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朊病毒感染小鼠海马内胶质纤维酸性蛋白片段表达增加及微钙蛋白酶激活。

Increased expression of glial fibrillary acidic protein fragments and mu-calpain activation within the hippocampus of prion-infected mice.

作者信息

Gray B C, Skipp P, O'Connor V M, Perry V H

机构信息

Neurosciences Group, School of Biological Sciences, University of Southampton, Southampton SO16 7PX, UK.

出版信息

Biochem Soc Trans. 2006 Feb;34(Pt 1):51-4. doi: 10.1042/BST0340051.

DOI:10.1042/BST0340051
PMID:16417481
Abstract

Prion diseases are characteristically accompanied by marked astrocytic activation, which is initiated relatively early in the disease process. Using the intracerebrally injected ME7 strain of prion agent to model disease, we identified an expected increase in GFAP (glial fibrillary acidic protein) but additionally noted an accumulation of GFAP cleavage fragments in hippocampal homogenates. A time-dependent increase in hippocampal mu-calpain immunoreactivity within astrocytes suggests that its proteolytic activity may account for the cleavage of GFAP that is observed in the ME7 model. It may therefore contribute to the reactive gliosis that is characteristic of prion diseases.

摘要

朊病毒疾病的特征是伴有显著的星形胶质细胞激活,这种激活在疾病过程中相对较早开始。使用脑内注射朊病毒制剂的ME7株来模拟疾病,我们发现胶质纤维酸性蛋白(GFAP)预期增加,但还注意到海马匀浆中GFAP裂解片段的积累。星形胶质细胞内海马μ-钙蛋白酶免疫反应性随时间的增加表明,其蛋白水解活性可能是ME7模型中观察到的GFAP裂解的原因。因此,它可能导致了朊病毒疾病所特有的反应性胶质增生。

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