The effects of amyloid-beta(42) oligomer on the proliferation and activation of astrocytes in vitro

文献类型： 外文期刊

第一作者： Hou, Lingling

作者： Hou, Lingling;Liu, Yanfeng;Wang, Xiaoyu;Ma, Haibin;He, Jinsheng;Zhang, Ying;Yu, Changhai;Guan, Weijun;Ma, Yuehui

作者机构：

关键词： Alzheimer's disease;Astrocyte;beta-amyloid (A beta(42)) peptide;Proliferation;Activation

期刊名称：IN VITRO CELLULAR & DEVELOPMENTAL BIOLOGY-ANIMAL （ 影响因子：2.416； 五年影响因子：2.117 ）

ISSN： 1071-2690

年卷期： 2011 年 47 卷 8 期

页码：

收录情况： SCI

摘要： Previous studies reported that astrocyte response to amyloid-beta (A beta) before obvious neuronal damage could be detected in Alzheimer's disease (AD). It is suggested that astrocytes play a key role in AD pathologies. In this study, we investigated the effects of A beta(42) oligomer on the proliferation and activation of astrocytes by in vitro experiments. The results showed that A beta(42) oligomers could convert astrocytes to responsive astrocytes. It was revealed by MTT and ELISA assays that the viability of astrocytes gradually decreased, and the release of brain-derived neurotrophic factor increased with elevated A beta(42) concentration and prolonged duration. Reverse-transcription polymerase chain reaction (RT-PCR) assay indicated that A beta(42) oligomers increased the expression of glial fibers acid protein and interleukin-1 beta in a dose-dependent but not time-dependent manner. It was showed that A8, a mouse monoclonal antibody, was able to protect the cultured astrocytes against the toxicity of A beta(42) oligomers. The result demonstrated that A8 could inhibit A beta(42) oligomers toxic effects on astrocytes and that, alone, A8 could promote the proliferation of astrocytes in certain time. The present study laid a theoretical foundation for further understanding the effects of A beta(42) on astrocytes and, hence, is conducive to the theoretical understanding and clinical therapies of AD progression.

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