Regulation of Microglia Identity from an Epigenetic and Transcriptomic Point of View

被引:17
|
作者
Eggen, Bart J. L. [1 ]
Boddeke, Erik W. G. M. [1 ]
Kooistra, Susanne M. [1 ]
机构
[1] Univ Groningen, Univ Med Ctr Groningen, Sect Med Physiol, Dept Neurosci, Antonius Deusinglaan 1, NL-9713 AV Groningen, Netherlands
关键词
microglia; transcriptome; chromatin; turnover; heterogeneity; CNS disease; PLURIPOTENT STEM-CELLS; MYELOID CELLS; FRACTALKINE RECEPTOR; MOUSE MODELS; GLIAL-CELLS; BRAIN; REVEALS; MACROPHAGES; SYSTEM; FATE;
D O I
10.1016/j.neuroscience.2017.12.010
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Microglia have long been recognized as the endogenous innate immune elements in the central nervous system (CNS) parenchyma. Besides fulfilling local immune-related functions, they provide cross-talk between the CNS and the immune system at large. In the adult CNS, microglia are involved in maintaining brain homeostasis, modulating synaptic transmission and clearance of apoptotic cells. During embryonic development, microglia are responsible for the removal of supernumerary synapses and neurons, and neuronal network formation. The full scale of their potential abilities has been highlighted by improvements in microglia isolation methods, the development of genetically tagged mouse models, advanced imaging technologies and the application of next-generation sequencing in recent years. Genome-wide expression analysis of relatively pure microglia populations from both mouse and human CNS tissues has thereby greatly contributed to our knowledge of their biology; what defines them under homeostatic conditions and how microglia respond to processes like aging and CNS disease? How and to what degree beneficial functions of microglia can be restored in the aged or diseased brain will be the key issue to be addressed in future research. This article is part of a Special Issue entitled: Microglia-Neuron interactions in health and disease - novel perspectives for translational research. (C) 2017 IBRO. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:3 / 13
页数:11
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