Increased expression of miRNA-146a in Alzheimer's disease transgenic mouse models

被引:109
作者
Li, Y. Y. [1 ,2 ]
Cui, J. G. [1 ,2 ]
Hill, J. M. [1 ,2 ,3 ,4 ,5 ]
Bhattacharjee, S. [1 ,2 ]
Zhao, Y. [6 ]
Lukiw, W. J. [1 ,2 ,5 ]
机构
[1] Louisiana State Univ, Hlth Sci Ctr, LSU Neurosci Ctr, New Orleans, LA 70112 USA
[2] Louisiana State Univ, Hlth Sci Ctr, Dept Ophthalmol, New Orleans, LA 70112 USA
[3] Louisiana State Univ, Hlth Sci Ctr, Dept Pharmacol, New Orleans, LA 70112 USA
[4] Louisiana State Univ, Hlth Sci Ctr, Dept Microbiol, New Orleans, LA 70112 USA
[5] Louisiana State Univ, Hlth Sci Ctr, Dept Genet, New Orleans, LA 70112 USA
[6] Univ Pittsburgh, Dept Biol Struct, Pittsburgh, PA 15260 USA
关键词
5xFAD; Alzheimer's disease; CAY10512; Curcumin; miRNA-146a; Neurodegeneration; NF-KB; PDTC; Tg2576; Transgenic models of Alzheimer's disease; AMYLOID DEPOSITION; SYNAPSE PATHOLOGY; PRECURSOR-PROTEIN; BETA; MICE; PLAQUES; MUTANT; TG2576; PRESENILIN-1; INDUCTION;
D O I
10.1016/j.neulet.2010.09.079
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
A mouse and human brain-enriched micro-RNA-146a (miRNA-146a) is known to be important in modulating the innate immune response and inflammatory signaling in certain immunological and brain cell types. In this study we examined miRNA-146a levels in early-, moderate- and late-stage Alzheimer's disease (AD) neocortex and hippocampus, in several human primary brain and retinal cell lines, and in 5 different transgenic mouse models of AD including Tg2576, TgCRND8, PSAPP, 3xTg-AD and 5xFAD. Inducible expression of miRNA-146a was found to be significantly up-regulated in a primary co-culture of human neuronal-glial (HNG) cells stressed using interleukin1-beta (IL-1 beta), and this up-regulation was quenched using specific NF-kB inhibitors including curcumin. Expression of miRNA-146a correlated with senile plaque density and synaptic pathology in Tg2576 and in 5xFAD transgenic mouse models used in the study of this common neurodegenerative disorder. (C) 2010 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:94 / 98
页数:5
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