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Neurosci Lett. 2011 Jul 20;499(2):109-13. doi: 10.1016/j.neulet.2011.05.044. Epub 2011 May 26.

Differential expression of miRNA-146a-regulated inflammatory genes in human primary neural, astroglial and microglial cells.

Author information

1
LSU Neuroscience Center, Department of Ophthalmology, Louisiana State University Health Science Center, New Orleans, LA 70112, USA.

Erratum in

  • Neurosci Lett. 2012 Jun 27;520(1):126.

Abstract

MicroRNA-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 Aβ42 peptide and tumor necrosis factor alpha (TNFα). 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 Aβ42-peptide+TNFα-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.

PMID:
21640790
PMCID:
PMC3713470
DOI:
10.1016/j.neulet.2011.05.044
[Indexed for MEDLINE]
Free PMC Article

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