{"id":1090,"date":"2022-04-02T05:55:00","date_gmt":"2022-04-02T05:55:00","guid":{"rendered":"https:\/\/www.ub.edu\/creatio\/wp\/?post_type=actualitat&#038;p=1090"},"modified":"2022-08-05T05:59:03","modified_gmt":"2022-08-05T05:59:03","slug":"alterationglycoprotein","status":"publish","type":"actualitat","link":"https:\/\/www.ub.edu\/creatio\/en\/news\/alterationglycoprotein\/","title":{"rendered":"Transmembrane Glycoprotein Alteration (Basic Research)"},"content":{"rendered":"\n<figure class=\"wp-block-image size-full\"><img loading=\"lazy\" decoding=\"async\" width=\"589\" height=\"392\" data-src=\"https:\/\/www.ub.edu\/creatio\/wp\/wp-content\/uploads\/2022\/08\/Alteracio-Glicoproteina-transmembrana_Recerca-Basica.png\" alt=\"Alteraci\u00f3 Glicoprote\u00efna transmembrana_Recerca B\u00e0sica\" class=\"wp-image-1087 lazyload\" data-srcset=\"https:\/\/www.ub.edu\/creatio\/wp-content\/uploads\/2022\/08\/Alteracio-Glicoproteina-transmembrana_Recerca-Basica.png 589w, https:\/\/www.ub.edu\/creatio\/wp-content\/uploads\/2022\/08\/Alteracio-Glicoproteina-transmembrana_Recerca-Basica-300x200.png 300w\" data-sizes=\"(max-width: 589px) 100vw, 589px\" src=\"data:image\/gif;base64,R0lGODlhAQABAAAAACH5BAEKAAEALAAAAAABAAEAAAICTAEAOw==\" style=\"--smush-placeholder-width: 589px; --smush-placeholder-aspect-ratio: 589\/392;\" \/><noscript><img loading=\"lazy\" decoding=\"async\" width=\"589\" height=\"392\" src=\"https:\/\/www.ub.edu\/creatio\/wp\/wp-content\/uploads\/2022\/08\/Alteracio-Glicoproteina-transmembrana_Recerca-Basica.png\" alt=\"Alteraci\u00f3 Glicoprote\u00efna transmembrana_Recerca B\u00e0sica\" class=\"wp-image-1087\" srcset=\"https:\/\/www.ub.edu\/creatio\/wp-content\/uploads\/2022\/08\/Alteracio-Glicoproteina-transmembrana_Recerca-Basica.png 589w, https:\/\/www.ub.edu\/creatio\/wp-content\/uploads\/2022\/08\/Alteracio-Glicoproteina-transmembrana_Recerca-Basica-300x200.png 300w\" sizes=\"(max-width: 589px) 100vw, 589px\" \/><\/noscript><\/figure>\n\n\n\n<h3 class=\"wp-block-heading\">Creatio\u2019s scientists describe, for the first time, dysregulation in the off-signaling between neurons and microglia in Huntington\u2019s disease (HD). <\/h3>\n\n\n\n<p>In the paper recently published by <a href=\"https:\/\/www.ncbi.nlm.nih.gov\/pubmed\/31790427\">Comella et al.<\/a>, we describe alterations in the temporal expression pattern of CD200-CD200R1 in both the CNS and blood in a transgenic mouse model of HD, the R6\/1. In a healthy brain, neuro-microglia crosstalk is maintained through different signaling pathways, notably through the interaction between the transmembrane glycoprotein ligand CD200 and its receptor CD200R1. The CD200-CD200R1 system is often altered in animal models of physiological aging or neurological disorders (such as multiple sclerosis, Parkinson\u2019s disease, depression, stress, and CNS infections) and in neurological symptoms of peripheral immune system activation. Hence, due to the lack of knowledge about neuronal-microglial communication in HD, and specifically about the CD200-CD200R1 system, Creatio prompted to investigate the expression of both the ligand and the receptor in HD mouse models to provide further insight into the function of the neuroimmune system in HD.<\/p>\n\n\n\n<p>Comella and coworkers demonstrated an increase in CD200 gene expression and protein levels in the brain parenchyma along with HD pathogenesis progression in R6\/1 mice. Interestingly, the expression of CD200 mRNA was also up-regulated in peripheral blood following a similar temporal pattern than the CD200 levels observed in the CNS. No alterations of CD200R1 expression were detected, suggesting that canonical neuro-microglial communication through CD200-CD200R1 interaction is not compromised, and that CD200 up-regulation in R6\/1 brain parenchyma could represent a neurotrophic signal to sustain or extend neuronal function in the latest stages of HD as a pro-survival mechanism.<\/p>\n\n\n\n<p>Creatio is confident in continuing this research line regarding the study of neuro-microglia interactions, particularly the CD200 as a possible pro-survival mechanism in HD pathogenesis. Elucidating the mechanisms of the interactions between neurons and microglia will provide novel therapeutic strategies to treat HD, a neurodegenerative condition with no effective, available therapy at the moment.<\/p>\n","protected":false},"author":1,"featured_media":1087,"template":"","acf":[],"yoast_head":"<!-- This site is optimized with the Yoast SEO plugin v22.7 - https:\/\/yoast.com\/wordpress\/plugins\/seo\/ -->\n<title>Transmembrane Glycoprotein Alteration (Basic Research) - Creatio<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/www.ub.edu\/creatio\/en\/news\/alterationglycoprotein\/\" \/>\n<meta property=\"og:locale\" content=\"es_ES\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Transmembrane Glycoprotein Alteration (Basic Research) - Creatio\" \/>\n<meta property=\"og:description\" content=\"Creatio\u2019s scientists describe, for the first time, dysregulation in the off-signaling between neurons and microglia in Huntington\u2019s disease (HD). In the paper recently published by Comella et al., we describe alterations in the temporal expression pattern of CD200-CD200R1 in both the CNS and blood in a transgenic mouse model of HD, the R6\/1. 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