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A neurodegeneration-specific gene-expression signature of acutely isolated microglia from an amyotrophic lateral sclerosis mouse model.

Abstract：

:Microglia are resident immune cells of the CNS that are activated by infection, neuronal injury, and inflammation. Here, we utilize flow cytometry and deep RNA sequencing of acutely isolated spinal cord microglia to define their activation in vivo. Analysis of resting microglia identified 29 genes that distinguish microglia from other CNS cells and peripheral macrophages/monocytes. We then analyzed molecular changes in microglia during neurodegenerative disease activation using the SOD1(G93A) mouse model of amyotrophic lateral sclerosis (ALS). We found that SOD1(G93A) microglia are not derived from infiltrating monocytes, and that both potentially neuroprotective and toxic factors, including Alzheimer's disease genes, are concurrently upregulated. Mutant microglia differed from SOD1(WT), lipopolysaccharide-activated microglia, and M1/M2 macrophages, defining an ALS-specific phenotype. Concurrent messenger RNA/fluorescence-activated cell sorting analysis revealed posttranscriptional regulation of microglia surface receptors and T cell-associated changes in the transcriptome. These results provide insights into microglia biology and establish a resource for future studies of neuroinflammation.

journal_name

Cell Rep

journal_title

Cell reports

authors

Chiu IM,Morimoto ET,Goodarzi H,Liao JT,O'Keeffe S,Phatnani HP,Muratet M,Carroll MC,Levy S,Tavazoie S,Myers RM,Maniatis T

doi

10.1016/j.celrep.2013.06.018

subject

Has Abstract

pub_date

2013-07-25 00:00:00

pages

385-401

issue

2

issn

2211-1247

pii

S2211-1247(13)00296-9

journal_volume

4

pub_type

杂志文章

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