The cytokine and endocannabinoid systems are co-regulated by NF-κB p65/RelA in cell culture and transgenic mouse models of Huntington's disease and in striatal tissue from Huntington's disease patients.

Abstract:

:Transcriptional dysregulation is a major pathological feature of Huntington's disease (HD). The goal of this study was to understand how p65/RelA co-regulated genes, specifically those of the cytokine and endocannabinoid systems, were affected in HD. p65/RelA levels were lower in human HD tissue and R6/2 HD mice, as were the levels of the type 1 cannabinoid receptor (CB1), IL-1β, IL-8, CCL5, GM-CSF, MIP-1β, and TNFα, all of which may be regulated by p65/RelA. Activation of p65/RelA restored CB1 and CCL5 expression in STHdh cell models of HD. Therefore, p65/RelA activation may normalize the expression of some genes in HD.

journal_name

J Neuroimmunol

authors

Laprairie RB,Warford JR,Hutchings S,Robertson GS,Kelly ME,Denovan-Wright EM

doi

10.1016/j.jneuroim.2013.12.008

subject

Has Abstract

pub_date

2014-02-15 00:00:00

pages

61-72

issue

1-2

eissn

0165-5728

issn

1872-8421

pii

S0165-5728(13)00339-1

journal_volume

267

pub_type

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