CD200 is up-regulated in R6/1 transgenic mouse model of Huntington's disease


Autoři: Andrea Comella Bolla aff001;  Tony Valente aff003;  Andres Miguez aff001;  Veronica Brito aff002;  Silvia Gines aff002;  Carme Solà aff003;  Marco Straccia aff001;  Josep M. Canals aff001
Působiště autorů: Stem Cells and Regenerative Medicine Laboratory, Production and Validation Center of Advanced Therapies (Creatio), Department of Biomedicine, Faculty of Medicine and Health Science, University of Barcelona, Barcelona, Spain aff001;  Neuroscience Institute, University of Barcelona, Barcelona, Spain aff002;  August Pi i Sunyer Biomedical Research Institute (IDIBAPS), Barcelona, Spain aff003;  Network Center for Biomedical Research in Neurodegenerative Diseases (CIBERNED), Madrid, Spain aff004;  Department of Cerebral Ischemia and Neurodegeneration, Institut d’Investigacions Biomèdiques de Barcelona–Consejo Superior de Investigaciones Científicas (IIBB–CSIC), Barcelona, Spain aff005;  Department of Biomedicine, Faculty of Medicine and Health Science, University of Barcelona, Barcelona, Spain aff006
Vyšlo v časopise: PLoS ONE 14(12)
Kategorie: Research Article
doi: 10.1371/journal.pone.0224901

Souhrn

In Huntington’s disease (HD), striatal medium spiny neurons (MSNs) are particularly sensitive to the presence of a CAG repeat in the huntingtin (HTT) gene. However, there are many evidences that cells from the peripheral immune system and central nervous system (CNS) immune cells, namely microglia, play an important role in the etiology and the progression of HD. However, it remains unclear whether MSNs neurodegeneration is mediated by a non-cell autonomous mechanism. The homeostasis in the healthy CNS is maintained by several mechanisms of interaction between all brain cells. Neurons can control microglia activation through several inhibitory mechanisms, such as the CD200–CD200R1 interaction. Due to the complete lack of knowledge about the CD200–CD200R1 system in HD, we determined the temporal patterns of CD200 and CD200R1 expression in the neocortex, hippocampus and striatum in the HD mouse models R6/1 and HdhQ111/7 from pre-symptomatic to manifest stages. In order to explore any alteration in the peripheral immune system, we also studied the levels of expression of CD200 and CD200R1 in whole blood. Although CD200R1 expression was not altered, we observed and increase in CD200 gene expression and protein levels in the brain parenchyma of all the regions we examined, along with HD pathogenesis in R6/1 mice. Interestingly, the expression of CD200 mRNA was also up-regulated in blood following a similar temporal pattern. These results suggest that canonical neuronal–microglial communication through CD200–CD200R1 interaction is not compromised, and 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 pro-survival mechanism.

Klíčová slova:

Blood – Central nervous system – Gene expression – Hippocampus – Microglial cells – Mouse models – Neostriatum – Neocortex


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