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

Robert B. Laprairie; Jordan R. Warford; Sarah Hutchings; George S. Robertson; Melanie E.M. Kelly; Eileen M. Denovan-Wright

doi:10.1016/j.jneuroim.2013.12.008

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

Robert B. Laprairie, Jordan R. Warford, Sarah Hutchings, George S. Robertson, Melanie E.M. Kelly, Eileen M. Denovan-Wright

Medicine

Producción científica: Contribución a una revista › Artículo › revisión exhaustiva

15 Citas (Scopus)

Resumen

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.

Idioma original	English
Páginas (desde-hasta)	61-72
Número de páginas	12
Publicación	Journal of Neuroimmunology
Volumen	267
N.º	1-2
DOI	https://doi.org/10.1016/j.jneuroim.2013.12.008
Estado	Published - 2014

Nota bibliográfica

Funding Information:
We thank Kathleen Murphy, for technical assistance during the preparation of this manuscript. We also thank the Canadian Institutes of Health Research (CIHR) , the Killam Trusts Foundation , the Huntington Society of Canada , Nova Scotia Health Research Foundation (NSHRF) , and the Canadian Consortium for the Investigation of Cannabinoids (CCIC) for funding this research.

ASJC Scopus Subject Areas

Immunology and Allergy
Immunology
Neurology
Clinical Neurology

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Laprairie, R. B., Warford, J. R., Hutchings, S., Robertson, G. S., Kelly, M. E. M., & Denovan-Wright, E. M. (2014). 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. Journal of Neuroimmunology, 267(1-2), 61-72. https://doi.org/10.1016/j.jneuroim.2013.12.008

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. / Laprairie, Robert B.; Warford, Jordan R.; Hutchings, Sarah et al.
En: Journal of Neuroimmunology, Vol. 267, N.º 1-2, 2014, p. 61-72.

Producción científica: Contribución a una revista › Artículo › revisión exhaustiva

Laprairie, RB, Warford, JR, Hutchings, S, Robertson, GS , Kelly, MEM & Denovan-Wright, EM 2014, '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', Journal of Neuroimmunology, vol. 267, n.º 1-2, pp. 61-72. https://doi.org/10.1016/j.jneuroim.2013.12.008

Laprairie RB, Warford JR, Hutchings S, Robertson GS , Kelly MEM , Denovan-Wright EM. 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. Journal of Neuroimmunology. 2014;267(1-2):61-72. doi: 10.1016/j.jneuroim.2013.12.008

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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.",

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note = "Funding Information: We thank Kathleen Murphy, for technical assistance during the preparation of this manuscript. We also thank the Canadian Institutes of Health Research (CIHR) , the Killam Trusts Foundation , the Huntington Society of Canada , Nova Scotia Health Research Foundation (NSHRF) , and the Canadian Consortium for the Investigation of Cannabinoids (CCIC) for funding this research. ",

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