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

Résultat de recherche: Article › examen par les pairs

15 Citations (Scopus)

Résumé

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.

Langue d'origine	English
Pages (de-à)	61-72
Nombre de pages	12
Journal	Journal of Neuroimmunology
Volume	267
Numéro de publication	1-2
DOI	https://doi.org/10.1016/j.jneuroim.2013.12.008
Statut de publication	Published - 2014

Note bibliographique

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

ODD de l’ONU

Cette action contribue à la réalisation des objectifs de développement durable suivants

Accès au document

10.1016/j.jneuroim.2013.12.008

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Citer

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.
Dans: Journal of Neuroimmunology, Vol. 267, N° 1-2, 2014, p. 61-72.

Résultat de recherche: Article › examen par les pairs

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° 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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