Aβ-Induced Repressor Element 1-Silencing Transcription Factor (REST) Gene Delivery Suppresses Activation of Microglia-Like BV-2 Cells
Compelling evidence from basic molecular biology has demonstrated the crucial role of microglia in the pathogenesis of Alzheimer’s disease (AD). Microglia were believed to play a dual role in both promoting and inhibiting Alzheimer’s disease progression. It is of great significance to regulate the f...
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Main Authors: | , , , , , , , , |
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Format: | Article |
Language: | English |
Published: |
Wiley
2020-01-01
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Series: | Neural Plasticity |
Online Access: | http://dx.doi.org/10.1155/2020/8888871 |
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Summary: | Compelling evidence from basic molecular biology has demonstrated the crucial role of microglia in the pathogenesis of Alzheimer’s disease (AD). Microglia were believed to play a dual role in both promoting and inhibiting Alzheimer’s disease progression. It is of great significance to regulate the function of microglia and make them develop in a favorable way. In the present study, we investigated the function of repressor element 1-silencing transcription factor (REST) in Aβ1-42-induced BV-2 cell dysfunction. We concluded that Aβ1-42 could promote type I activation of BV-2 cells and induce cell proliferation, migration, and proinflammation cytokine TNF-α, IL-1β, and IL-6 expression. Meanwhile, REST was upregulated, and nuclear translocalization took place due to Aβ1-42 stimulation. When REST was knocked down by a specific short hairpin RNA (sh-RNA), BV-2 cell proliferation, migration, and proinflammation cytokine expression and secretion induced by Aβ1-42 were increased, demonstrating that REST may act as a repressor of microglia-like BV-2 cell activation. |
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ISSN: | 2090-5904 1687-5443 |