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

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journal contribution
posted on 2019-06-17, 10:57 authored by G Kronenberg, R Uhlemann, J Schöner, S Wegner, V Boujon, N Deigendesch, M Endres, K Gertz
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.

Funding

This work was supported by the Deutsche Forschungsgemeinschaft (GE2576/3-1 to K.G; DFG KR2956/5-1 to G.K; Exc257 to M.E.), the Bundesministerium für Bildung und Forschung (Center for Stroke Research Berlin to G.K., K.G. and M.E.), the European Union’s Seventh Framework Programme (FP7/HEALTH.2013.2.4.2-1) under grant agreement n° 602354 (Counterstroke consortium to K.G. and M.E.), the German Center for Neurodegenerative Disease (DZNE to M.E.), the German Center for Cardiovascular Research (DZHK to M.E.), and the Corona Foundation (to M.E.).

History

Citation

European Archives of Psychiatry and Clinical Neuroscience, 2017, 267 (5), pp. 473-477

Author affiliation

/Organisation/COLLEGE OF LIFE SCIENCES/School of Medicine/Department of Cardiovascular Sciences

Version

  • VoR (Version of Record)

Published in

European Archives of Psychiatry and Clinical Neuroscience

Publisher

Springer (part of Springer Nature)

eissn

1433-8491

Acceptance date

2016-11-18

Copyright date

2016

Available date

2019-06-17

Publisher DOI

Publisher version

https://link.springer.com/article/10.1007/s00406-016-0750-1

Language

en

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    University of Leicester Publications

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    Keywords

    Alzheimer’s diseaseMicrogliaMitochondrial biogenesisNeurodegenerative diseaseTelomeraseAnimalsCD11b AntigenCell PolarityCells, CulturedCyclin-Dependent Kinase Inhibitor p21CytokinesDisease Models, AnimalGene Expression RegulationInfarction, Middle Cerebral ArteryLipopolysaccharidesMaleMiceMice, Inbred C57BLMice, TransgenicMutationNF-E2-Related Factor 2Presenilin-1RNA, Messenger

    Licence

    CC BY 4.0

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