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

页码：473 / 477

页数：5

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