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

被引：16
|
作者：
Kronenberg, Golo [1 ,2 ,3 ,4 ]
Uhlemann, Ria [2 ,3 ]
Schoener, Johanna [1 ,2 ,3 ]
Wegner, Stephanie [2 ,3 ]
Boujon, Valerie [2 ,3 ]
Deigendesch, Nikolas [5 ]
Endres, Matthias [2 ,3 ,6 ,7 ,8 ]
Gertz, Karen [2 ,3 ]
机构：
[1] Charite Campus Mitte, Klin Psychiat & Psychotherapie, Berlin, Germany
[2] Charite, Ctr Stroke Res Berlin CSB, Berlin, Germany
[3] Charite, Klin & Hochschulambulanz Neurol, Berlin, Germany
[4] Univ Med Rostock, Klin & Poliklin Psychiat & Psychotherapie, Gehlsheimer Str 20, D-18147 Rostock, Germany
[5] Charite, Inst Neuropathol, Berlin, Germany
[6] German Ctr Neurodegenerat Dis DZNE, Charitepl 1, D-10117 Berlin, Germany
[7] Charite, Cluster Excellence NeuroCure, Berlin, Germany
[8] DZHK German Ctr Cardiovasc Res, Partner Site Berlin,Charitepl 1, D-10117 Berlin, Germany
来源：
EUROPEAN ARCHIVES OF PSYCHIATRY AND CLINICAL NEUROSCIENCE | 2017年 / 267卷 / 05期
关键词：
Alzheimer's disease; Microglia; Mitochondrial biogenesis; Neurodegenerative disease; Telomerase; ENDOTHELIAL FUNCTION; MICE; STROKE; CELLS;
D O I：
10.1007/s00406-016-0750-1
中图分类号：
R74 [神经病学与精神病学];
学科分类号：
摘要：
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.
引用
收藏
页码：473 / 477
页数：5
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