Gene Expression Analysis of Astrocyte and Microglia Endocannabinoid Signaling during Autoimmune Demyelination
dc.contributor.author | Moreno García, Álvaro | |
dc.contributor.author | Bernal Chico, Ana | |
dc.contributor.author | Colomer, Teresa | |
dc.contributor.author | Rodríguez-Antigüedad Zarranz, Alfredo | |
dc.contributor.author | Matute Almau, Carlos José | |
dc.contributor.author | Mato Santos, Susana | |
dc.date.accessioned | 2020-10-01T10:58:08Z | |
dc.date.available | 2020-10-01T10:58:08Z | |
dc.date.issued | 2020-08-24 | |
dc.identifier.citation | Biomolecules 10(9) : (2020) // Article ID 1228 | es_ES |
dc.identifier.issn | 2218-273X | |
dc.identifier.uri | http://hdl.handle.net/10810/46334 | |
dc.description.abstract | The endocannabinoid system is associated with protective effects in multiple sclerosis (MS) that involve attenuated innate immune cell responses. Astrocytes and microglia are modulated by endocannabinoids and participate in the biosynthesis and metabolism of these compounds. However, the role of neuroglial cells as targets and mediators of endocannabinoid signaling in MS is poorly understood. Here we used a microfluidic RT-qPCR screen to assess changes in the expression of the main endocannabinoid signaling genes in astrocytes and microglia purified from female mice during the time-course of experimental autoimmune encephalomyelitis (EAE). We show that astrocytes and microglia upregulate the expression of genes encoding neurotoxic A1 and pro-inflammatory molecules at the acute disease with many of these transcripts remaining elevated during the recovery phase. Both cell populations exhibited an early onset decrease in the gene expression levels of 2-arachidonoylglycerol (2-AG) hydrolytic enzymes that persisted during EAE progression as well as cell-type-specific changes in the transcript levels for genes encoding cannabinoid receptors and molecules involved in anandamide (AEA) signaling. Our results demonstrate that astrocytes and microglia responses to autoimmune demyelination involve alterations in the expression of multiple endocannabinoid signaling-associated genes and suggest that this system may regulate the induction of neurotoxic and pro-inflammatory transcriptional programs in both cell types during MS. | es_ES |
dc.description.sponsorship | This research was funded by FEDER and ISCIII (AES 2018—PI18/00513 to S.M. and A.R.-A.), the Basque Government (PIBA19-0059 to S.M. and IT1203-19 to C.M.), the Spanish Ministry of Economy and Competitiveness (SAF2016-75292-R to C.M.) and CIBERNED (CB06/0005/0076 to C.M.). A.M.-G. and A.B.-C. held fellowships from the UPV/EHU and the Basque Government, respectively. | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | MDPI | es_ES |
dc.relation | info:eu-repo/grantAgreement/MINECO/SAF2016-75292-R to C.M. | es_ES |
dc.rights | info:eu-repo/semantics/openAccess | es_ES |
dc.rights.uri | http://creativecommons.org/licenses/by/3.0/es/ | |
dc.subject | multiple sclerosis | es_ES |
dc.subject | EAE | es_ES |
dc.subject | astrocytes | es_ES |
dc.subject | microglia | es_ES |
dc.subject | endocannabinoids | es_ES |
dc.title | Gene Expression Analysis of Astrocyte and Microglia Endocannabinoid Signaling during Autoimmune Demyelination | es_ES |
dc.type | info:eu-repo/semantics/article | es_ES |
dc.date.updated | 2020-09-25T13:26:47Z | |
dc.rights.holder | 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). | es_ES |
dc.relation.publisherversion | https://www.mdpi.com/2218-273X/10/9/1228 | es_ES |
dc.identifier.doi | 10.3390/biom10091228 | |
dc.departamentoes | Neurociencias | |
dc.departamentoeu | Neurozientziak |
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Except where otherwise noted, this item's license is described as 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).