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C/EBPβ expression in activated microglia in amyotrophic lateral sclerosis.

Abstract：

:Neuroinflammation is thought to play a pathogenic role in many neurodegenerative disorders including amyotrophic lateral sclerosis (ALS). In this study we demonstrate that the expression of nitric oxide (NO) synthase-2 (NOS2), and cyclooxygenase (COX)-2 induced by lipopolysaccharide (LPS) with interferon-γ is higher in microglial-enriched cultures from G93A-SOD1 mice, an ALS animal model, than from wild type mice. The levels of CCAAT/enhancer binding protein β (C/EBPβ), a transcription factor that regulates proinflammatory gene expression, are also upregulated in activated G93A-SOD1 microglial cells. In vivo, systemic lipopolysaccharide also induces an exacerbated neuroinflammatory response in G93A-SOD1 mice versus wild type mice, with increased expression of glial fibrillary acidic protein (GFAP), CD11b, nitric oxide synthase-2, cyclooxygenase-2, proinflammatory cytokines, and C/EBPβ. Finally, we report that C/EBPβ is expressed by microglia in the spinal cord of ALS patients. This is the first demonstration to our knowledge of microglial C/EBPβ expression in human disease. Altogether these findings indicate that G93A-SOD1 expression results in an exacerbated pattern of neuroinflammation and suggest that C/EBPβ is a candidate to regulate the expression of potentially neurotoxic genes in microglial cells in ALS.

journal_name

Neurobiol Aging

journal_title

Neurobiology of aging

authors

Valente T,Mancera P,Tusell JM,Serratosa J,Saura J

doi

10.1016/j.neurobiolaging.2011.09.019

subject

Has Abstract

pub_date

2012-09-01 00:00:00

pages

2186-99

issue

9

eissn

0197-4580

issn

1558-1497

pii

S0197-4580(11)00356-3

journal_volume

33

pub_type

杂志文章

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