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Role of nitric oxide produced by iNOS through NF-κB pathway in migration of cerebellar granule neurons induced by Lipopolysaccharide.

Abstract：

:Inflammatory stimulus during development increases the risk for adverse neurologic outcome. One possible mechanism is disrupting neuronal migration. Using lipopolysaccharide (LPS)-treatment to assess inflammatory stimulus on neuronal migration of cerebellar granule neurons, we previously found that LPS-activation increased the neuronal migration. The precise mechanisms behind these effects have not been investigated. Independently, it was shown that nitric oxide (NO(•-)) regulates neuronal migration during development, that NO(•-) is produced by inducible nitric oxide synthase (iNOS) in response to LPS through the activation of nuclear factor (NF)-κB, and that LPS induce the expression of genes under the transcriptional control of NF-κB in primary cultures from developing mouse cerebellum. To investigate the relationship between these events, we used this culture model to study the role of NO(•-) produced by iNOS through NF-κB signaling pathway, in the effect of LPS on neuron migration. LPS increased NO(•-) production, iNOS protein levels and NF-κB nuclear levels; concomitantly with NO(•-) production, LPS increased the neuronal migration as compared to non stimulated cultures. The necessary roles of the NO(•-) and iNOS were demonstrated by chelating of NO(•-) with hemoglobin and the inhibition of iNOS by 1400W. Each of these treatments reduced neuronal migration induced by LPS. The role of NF-κB was showed by using the inhibitor JSH-23, which decreased NO(•-) production and neuronal migration in LPS activated cultures. These results suggest that neuronal migration during development is susceptible to be modified by pro-inflammatory stimulus such as LPS through intracellular pathways associated with their receptors.

journal_name

Cell Signal

journal_title

Cellular signalling

authors

Arias-Salvatierra D,Silbergeld EK,Acosta-Saavedra LC,Calderon-Aranda ES

doi

10.1016/j.cellsig.2010.10.017

subject

Has Abstract

pub_date

2011-02-01 00:00:00

pages

425-35

issue

2

eissn

0898-6568

issn

1873-3913

pii

S0898-6568(10)00304-9

journal_volume

23

pub_type

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