Journal
SCIENCE
Volume 356, Issue 6344, Pages -Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aal3222
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Funding
- Larry L. Hillbloom Foundation
- NIH [NS096170, DK063491, GM085764]
- NIH-National Cancer Institute CCSG [P30 014195]
- Canadian Institutes of Health Research fellowship
- Multiple Sclerosis Society of Canada fellowship
- University of California, San Diego [T32DK007541]
- University Medical Center Groningen Institutional postdoctoral traveling grant
- Dutch MS Research Foundation
- Gemmy and Mibeth Tichelaar Foundation
- Deutsche Forschungsgemeinschaft [SCHL2102/1-1]
- European Molecular Biology Organization Long-term Fellowship
- Bettencourt-Schueller Foundation
- Philippe Foundation
- JPB Foundation
- Dolby Family Ventures
- Paul G. Allen Family Foundation
- Engman Foundation
- Ben and Wanda Hildyard Chair in Hereditary Diseases
- Flow Cytometry Core Facility of the Salk Institutes
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Microglia play essential roles in central nervous system (CNS) homeostasis and influence diverse aspects of neuronal function. However, the transcriptional mechanisms that specify human microglia phenotypes are largely unknown. We examined the transcriptomes and epigenetic landscapes of human microglia isolated from surgically resected brain tissue ex vivo and after transition to an in vitro environment. Transfer to a tissue culture environment resulted in rapid and extensive down-regulation of microglia-specific genes that were induced in primitive mouse macrophages after migration into the fetal brain. Substantial subsets of these genes exhibited altered expression in neurodegenerative and behavioral diseases and were associated with noncoding risk variants. These findings reveal an environment-dependent transcriptional network specifying microglia-specific programs of gene expression and facilitate efforts to understand the roles of microglia in human brain diseases.
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