期刊
NEUROSCIENCE LETTERS
卷 499, 期 2, 页码 109-113出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2011.05.044
关键词
Brain gene expression; Complement factor H (CFH); Human astroglial cells; Microglial cells; Interleukin-1 receptor associated kinase 1 (IRAK-1); microRNA (miRNA); Neurodegeneration; Neuroinflammation; Post-transcriptional control; Small RNA; Tetraspanin 12 (TSPAN12)
资金
- Louisiana State University Board of Regents
- Alzheimer Association [IIRG-09-131729]
- National Institutes of Health [NIA AG038834]
Micro RNA-146a (miRNA-146a) is an inducible, 22 nucleotide, small RNA over-expressed in Alzheimer's disease (AD) brain. Up-regulated miRNA-146a targets several inflammation-related and membrane-associated messenger RNAs (mRNAs), including those encoding complement factor-H (CFH) and the interleukin-1 receptor associated kinase-1 (IRAK-1), resulting in significant decreases in their expression (p < 0.05, ANOVA). In this study we assayed miRNA-146a, CFH, IRAK-1 and tetraspanin-12 (TSPAN12), abundances in primary human neuronal-glial (HNG) co-cultures, in human astroglial (HAG) and microglial (HMG) cells stressed with A beta 42 peptide and tumor necrosis factor alpha (TNF alpha). The results indicate a consistent inverse relationship between miRNA-146a and CFH, IRAK-1 and TSPAN12 expression levels, and indicate that HNG, HAG and HMG cell types each respond differently to A beta 42-peptide + TNF alpha-triggered stress. While the strongest miRNA-146a-IRAK-1 response was found in HAG cells, the largest miRNA-146a-TSPAN12 response was found in HNG cells, and the most significant miRNA-146a-CFH changes were found in HMG cells, the 'resident scavenging macrophages' of the brain. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
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