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

详细信息    查看全文

• 作者：Robert B. Laprairie ; Jordan R. Warford ; Sarah Hutchings ; George S. Robertson ; Melanie E.M. Kelly ; Eileen M. Denovan-Wright
• 关键词：Huntington's disease ; Neuroinflammation ; NF-魏B p65/RelA ; Cannabinoid ; Cytokine
• 刊名：Journal of Neuroimmunology
• 出版年：15 February, 2014
• 年：2014
• 卷：267
• 期：1-2
• 页码：61-72
• 全文大小：1507 K

文摘

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-1尾, IL-8, CCL5, GM-CSF, MIP-1尾, and TNF伪, 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.