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Repression of telomere-associated genes by microglia activation in neuropsychiatric disease

Microglia senescence may promote neuropsychiatric disease. This prompted us to examine the relationship between microglia activation states and telomere biology. A panel of candidate genes associated with telomere maintenance, mitochondrial biogenesis, and cell-cycle regulation were investigated in...

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Detalles Bibliográficos
Autores principales: Kronenberg, Golo, Uhlemann, Ria, Schöner, Johanna, Wegner, Stephanie, Boujon, Valérie, Deigendesch, Nikolas, Endres, Matthias, Gertz, Karen
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5509772/
https://www.ncbi.nlm.nih.gov/pubmed/27896432
http://dx.doi.org/10.1007/s00406-016-0750-1
Descripción
Sumario:Microglia senescence may promote neuropsychiatric disease. This prompted us to examine the relationship between microglia activation states and telomere biology. A panel of candidate genes associated with telomere maintenance, mitochondrial biogenesis, and cell-cycle regulation were investigated in M1- and M2-polarized microglia in vitro as well as in MACS-purified CD11b+ microglia/brain macrophages from models of stroke, Alzheimer’s disease, and chronic stress. M1 polarization, ischemia, and Alzheimer pathology elicited a strikingly similar transcriptomic profile with, in particular, reduced expression of murine Tert. Our results link classical microglia activation with repression of telomere-associated genes, suggesting a new mechanism underlying microglia dysfunction.