Methyl-CpG Binding Protein 2 Regulates Microglia and Macrophage Gene Expression in Response to Inflammatory Stimuli
Open accessAbstract
Mutations in MECP2, encoding the epigenetic regulator methyl-CpG-binding protein 2, are the predominant cause of Rett syndrome, a disease characterized by both neurological symptoms and systemic abnormalities. Microglial dysfunction is thought to contribute to disease pathogenesis, and here we found microglia become activated and subsequently lost with disease progression in Mecp2-null mice. Mecp2 was found to be expressed in peripheral macrophage and monocyte populations, several of which also became depleted in Mecp2-null mice. RNA-seq revealed increased expression of glucocorticoid- and hypoxia-induced transcripts in Mecp2-deficient microglia and peritoneal macrophages. Furthermore, Mecp2 was found to regulate inflammatory gene transcription in response to TNF stimulation. Postnatal re-expression of Mecp2 using Cx3cr1(creER) increased the lifespan of otherwise Mecp2-null mice. These data suggest that Mecp2 regulates microglia and macrophage responsiveness to environmental stimuli to promote homeostasis. Dysfunction of tissue-resident macrophages might contribute to the systemic pathologies observed in Rett syndrome.
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MeCP2 is essential for the functions of astrocytes and microglia.
“MeCP2 is also essential for the functions of astrocytes and microglia (176, 177).”
From Microglia Function in the Central Nervous System During Health and Neurodegeneration (2017) · cites this paper as [177]
Under pathological circumstances, cues such as debris or stress signals can cause transcriptomic and morphological changes in microglia, switching them from homeostatic to reactive states.
“Under pathological circumstances, cues such as debris or stress signals from surrounding tissue can lead to transcriptomic and morphological changes in microglia, which can switch from homeostatic to reactive states [16, 17].”
From Transcriptional and Epigenetic Regulation of Microglia in Health and Disease (2019) · cites this paper as [17]
Global loss of Mecp2 reduces numbers of microglia, perivascular meningeal macrophages, intestinal macrophages, and LY6Clo circulating monocytes.
“Global loss of Mecp2 leads to reduced numbers of microglia, perivascular meningeal macrophages, intestinal macrophages and LY6Clo circulating monocytes [17].”
From Transcriptional and Epigenetic Regulation of Microglia in Health and Disease (2019) · cites this paper as [17]
Mecp2 is critical for maintaining immune cell function including microglia.
“suggesting Mecp2 is critical for maintaining immune cell function including microglia [17].”
From Transcriptional and Epigenetic Regulation of Microglia in Health and Disease (2019) · cites this paper as [17]
MECP2 deficiency, as seen in Rett Syndrome, can lead to microglial activation and dysfunction.
“MECP2-deficiency, as seen in Rett Syndrome, can lead to microglial activation and dysfunction [17].”
From Transcriptional and Epigenetic Regulation of Microglia in Health and Disease (2019) · cites this paper as [17]
Mecp2 deletion dysregulates genes involved in glucocorticoid signaling, hypoxia response, and inflammatory responses.
“These results show dysregulation of genes involved in glucocorticoid signaling, hypoxia response and inflammatory responses, suggesting Mecp2 is critical for maintaining immune cell function including microglia [17].”
From Transcriptional and Epigenetic Regulation of Microglia in Health and Disease (2019) · cites this paper as [17]
ChIP-seq analysis revealed that Mecp2 deletion increased histone acetylation at enhancer regions of Fkbp5 and recruited NCOR2 and HDAC3 complex.
“Further examination with ChIP-seq analysis revealed that Mecp2-deletion increased histone acetylation at enhancer regions of Fkbp5, a canonical glucocorticoid target gene, and recruitment of nuclear receptor co-repressor2 (NCOR2) and HDAC3 complex [17].”
From Transcriptional and Epigenetic Regulation of Microglia in Health and Disease (2019) · cites this paper as [17]
MECP2 regulates microglial responsiveness to environmental stimuli.
“Methyl-CpG binding protein 2 (MECP2) regulates microglial responsiveness to environmental stimuli.”
From Transcriptional and Epigenetic Regulation of Microglia in Health and Disease (2019) · cites this paper as [17]
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- Maezawa I Jin LW Rett syndrome microglia damage dendrites and synapses by the elevated release of glutamate The Journal of neuroscience: the official journal of the Society for Neuroscience 2010 30 5346 5356 20392956 PMC5533099
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- Authors
- Cronk, J. C., Derecki, N. C., Ji, E., Xu, Y., Lampano, A. E., Smirnov, I., Baker, W., Norris, G. T., Marin, I., Coddington, N., Wolf, Y., Turner, S. D., Aderem, A., Klibanov, A. L., Harris, T. H., Jung, S., Litvak, V., & Kipnis, J.
- Affiliations
- University of Virginia Medical Center (US)
- University of Virginia (US)
- University of Massachusetts Chan Medical School (US)
- Weizmann Institute of Science (IL)
- Center for Infectious Disease Research (US)
- Corresponding author
- Litvak, Vladimir
- Kipnis, Jonathan
- ORCID
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2015-04
- Volume
- 42
- Issue
- 4
- Pages
- 679-691
- ISSN
- 1074-7613 (ISSN-L)
- PMC
- PMC4407145
- OpenAlex
- W2040889890
- Cited by
- 199
- References
- 48
- Citations by year
- 2026: 12 · 2025: 21 · 2024: 14 · 2023: 18 · 2022: 14 · 2021: 22 · 2020: 8 · 2019: 21 · 2018: 24 · 2017: 22 · 2016: 15 · 2015: 8
- FWCI
- 15.72
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Immunity (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of General Medical Sciences (T32GM007267)
- National Institute of Allergy and Infectious Diseases (U19AI100627, F30AI109984)
- National Institute of Neurological Disorders and Stroke (R01NS081026, NS081026)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Keywords
- MeCP2, Rett syndrome, microglia, macrophages, monocytes, microglial activation, inflammatory gene expression, TNF signaling, glucocorticoid response, hypoxia response, epigenetic regulation, Mecp2-null mice, lifespan, tissue homeostasis
- MeSH terms
- CX3C Chemokine Receptor 1, Animals, Disease Models, Animal, Female, Homeostasis, Humans, Longevity, Male, Mice, Inbred C57BL, Tumor Necrosis Factor-alpha, Signal Transduction, Rett Syndrome, Microglia, Macrophages, Peritoneal, Mice, Knockout, CpG Islands, DNA Methylation, Integrases, Receptors, Chemokine, Gene Expression Profiling, Epigenesis, Genetic, Mice, Methyl-CpG-Binding Protein 2, High-Throughput Nucleotide Sequencing
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