期刊
NEUROSCIENCE
卷 193, 期 -, 页码 330-337出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuroscience.2011.06.088
关键词
mesenchymal stem cells; Alzheimer's disease; truncated tau protein
资金
- Axon Neuroscience and research [VEGA 2/0144/08, VEGA 2/0067/10, VEGA 2/0204/11, VEGA 2/0161/11, VEGA 2/0193/11, LPP-0039-09, APVV 0631-07]
- structural fund [26240220046]
We have developed a stably transfected human cell model for Alzheimer's disease with doxycycline-inducible expression of human misfolded truncated tau protein (AT tau). We have showed that AT tau reduced the metabolic activity of the AT tau cells, slowed down cell proliferation, and induced caspase-3-independent apoptosis-like programmed cell death, tauoptosis. The aim of this study was to test the possible capability of rat mesenchymal stem cells (MSCs) to interfere with AT tau protein-induced cell death. AT tau cells after treatment with 10 mu M all-trans retinoic acid were either co-cultivated with MSCs or supplemented with MSC secretome for 6 and 9 days. We found that both MSCs and MSC secretome promoted survival and increased the metabolic activity of the cells. Moreover stem cells induced cell differentiation and formation of neurites with numerous varicosities. Strikingly, treatment had no effect on tau expression suggesting that MSC induced self-protecting mechanism that prevented AT tau cells from tauoptosis. Our results showed that mesenchymal stem cells and their secretome are able to rescue the Alzheimer's disease cell model from cell death induced by misfolded truncated tau. We suggest that cell therapy may represent an alternative therapeutic avenue for treatment of human Alzheimer's disease and related tauopathies. (C) 2011 IBRO. Published by Elsevier Ltd. 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