Abstract
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.
Highlights
Alzheimer’s disease (AD), a chronic and neurodegenerative disease, is currently the most prevalent cause of dementia of aging people
We evaluated the levels of repressor element 1-silencing transcription factor (REST) protein in Aβ1-42-treated BV-2 cells and characterized the effect of REST on the function of microglia including proliferation, cell migration, and expression and secretion of proinflammation cytokines
We investigated the effect of synthetic Aβ1-42 on BV-2 cell proliferation using the CCK8 assay
Summary
Alzheimer’s disease (AD), a chronic and neurodegenerative disease, is currently the most prevalent cause of dementia of aging people. The main innate immune cells in the central nervous system, play a pivotal role in the process of AD including secretion of proinflammation cytokines, clearance of amyloid plaques, and synaptic pruning [4,5,6]. REST is known to play a key role in neuronal differentiation, including neurogenesis, synaptogenesis, excitability, and synaptic transmission [9, 10]. REST dysregulation has been associated with neurodegenerative diseases, such as Alzheimer’s disease [11,12,13]. We evaluated the levels of REST protein in Aβ1-42-treated BV-2 cells and characterized the effect of REST on the function of microglia including proliferation, cell migration, and expression and secretion of proinflammation cytokines
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