References
- Gosselin D, Skola D, Coufal NG, et al. An environment-dependent transcriptional network specifies human microglia identity. Science. 2017 Jun 23;356(6344):6344.
- Lavin Y, Winter D, Blecher-Gonen R, et al. Tissue-resident macrophage enhancer landscapes are shaped by the local microenvironment. Cell. 2014;159(6):1312–19. doi: 10.1016/j.cell.2014.11.018
- Gosselin D, Link VM, Romanoski CE, et al. Environment drives selection and function of enhancers controlling tissue-specific macrophage identities. Cell. 2014;159(6):1327–1340. doi: 10.1016/j.cell.2014.11.023
- Prinz M, Masuda T, Wheeler MA, et al. Microglia and central nervous system–associated macrophages—from origin to disease modulation. Annual Reviews. 2021;39:251–277. doi: 10.1146/annurev-immunol-093019-110159
- Guerreiro R, Wojtas A, Bras J, et al. TREM2 variants in alzheimer’s disease. N Engl J Med. 2013;368(2):117–127. doi: 10.1056/NEJMoa1211851
- Hollingworth P, Harold D, Sims R, et al. Common variants at ABCA7, MS4A6A/MS4A4E, EPHA1, CD33 and CD2AP are associated with Alzheimer’s disease. Nature Genetics Nature Publishing Group. 2011;43:429–436. doi:10.1038/ng.803
- Sims R, Badarinarayan N, Raybould R, et al. Rare coding variants in PLCG2, ABI3 and TREM2 implicate microglial-mediated innate immunity in Alzheimer’s disease. Nature Genet. 2017;49(9):1373–1384. doi: 10.1038/ng.3916
- Sekar A, Bialas AR, De Rivera H, et al. Schizophrenia risk from complex variation of complement component 4. Nature. 2016;530:177–183. doi: 10.1038/nature16549
- Park TJ, Kim HJ, Kim JH, et al. Associations of CD6, TNFRSF1A and IRF8 polymorphisms with risk of inflammatory demyelinating diseases. Neuropathol Appl Neurobiol. 2013;39(5):519–530. doi: 10.1111/j.1365-2990.2012.01304.x
- Leppä V, Surakka I, Tienari PJ, et al. The genetic association of variants in CD6, TNFRSF1A and IRF8 to multiple sclerosis: a multicenter case-control study. PLoS One. 2011;6(4):6. doi: 10.1371/journal.pone.0018813
- De Jager PL, Jia X, Wang J, et al. Meta-analysis of genome scans and replication identify CD6, IRF8 and TNFRSF1A as new multiple sclerosis susceptibility loci. Nature Genetics Nat Genet. 2009;41(7):776–782. doi: 10.1038/ng.401
- Hammond TR, Robinton D, Stevens B. Microglia and the brain: complementary partners in development and disease. Annu Rev Cell Dev Biol. 2018;34:523–544.
- Kaikkonen MU, Spann NJ, Heinz S, et al. Remodeling of the enhancer landscape during macrophage activation is coupled to enhancer transcription. Molecular Cell Elsevier Inc. 2013;51(3):310–325. doi: 10.1016/j.molcel.2013.07.010
- Bannister AJ, Kouzarides T. Regulation of chromatin by histone modifications. Cell Res. 2011;21(3):381–395. doi: 10.1038/cr.2011.22
- Vogel Ciernia A, LaSalle J. The landscape of DNA methylation amid a perfect storm of autism aetiologies. Nat Rev Neurosci. 2016;6(7):411–423. doi: 10.1038/nrn.2016.41
- Rowland ME, Jajarmi JM, Osborne TSM, et al. Insights into the emerging role of Baf53b in autism spectrum disorder. Front Mol Neurosci. 2022;15:805158. doi: 10.3389/fnmol.2022.805158
- Vogel-Ciernia A, Wood M. Molecular brake pad hypothesis: pulling off the brakes for emotional memory. Rev Neurosci. 2012;23(5–6):607–626. doi: 10.1515/revneuro-2012-0050
- Talbert PB, Henikoff S. The Yin and Yang of histone marks in transcription. Ann Rev Genomics Hum Genet. 2021;22(1):147–170. doi: 10.1146/annurev-genom-120220-085159
- Suuronen T, Huuskonen J, Pihlaja R, et al. Regulation of microglial inflammatory response by histone deacetylase inhibitors. J Neurochem. 2003;87(2):407–416. doi: 10.1046/j.1471-4159.2003.02004.x
- Huuskonen J, Suuronen T, Nuutinen T, et al. Regulation of microglial inflammatory response by sodium butyrate and short-chain fatty acids. Br J Pharmacol. 2004;141(5):874–880. doi: 10.1038/sj.bjp.0705682
- Singh V, Bhatia HS, Kumar A, et al. Histone deacetylase inhibitors valproic acid and sodium butyrate enhance prostaglandins release in lipopolysaccharide-activated primary microglia. Neuroscience. 2014;265:147–157. doi: 10.1016/j.neuroscience.2014.01.037
- Durham BS, Grigg R, Wood IC. Inhibition of histone deacetylase 1 or 2 reduces induced cytokine expression in microglia through a protein synthesis independent mechanism. J Neurochem. 2017;143(2):214–224. doi: 10.1111/jnc.14144
- Kannan V, Brouwer N, Hanisch UK, et al. Histone deacetylase inhibitors suppress immune activation in primary mouse microglia. Journal Of Neuroscience Research J Neurosci Res. 2013;91:1133–1142.
- Suh H-S, Choi S, Khattar P, et al. Histone deacetylase inhibitors suppress the expression of inflammatory and innate immune response genes in human microglia and astrocytes. J Neuroimmune Pharmacol. 2010;5(4):521–532. doi: 10.1007/s11481-010-9192-0
- Hsing CH, Hung SK, Chen YC, et al. Histone deacetylase inhibitor trichostatin a ameliorated endotoxin-induced neuroinflammation and cognitive dysfunction. 2015. doi: 10.1155/2015/163140
- Bian HT, Xiao L, Liang L, et al. RGFP966 is protective against lipopolysaccharide-induced depressive-like behaviors in mice by inhibiting neuroinflammation and microglial activation. Int Immunopharmacol. 2021;101:108259. Accessed December 2, 2021. online serial online serial. doi: 10.1016/j.intimp.2021.108259
- Zhang MJ, Zhao QC, Xia MX, et al. The HDAC3 inhibitor RGFP966 ameliorated ischemic brain damage by downregulating the AIM2 inflammasome. Faseb J. 2020;34(1):648–662. John Wiley and Sons Inc. doi: 10.1096/fj.201900394RRR
- Kuboyama T, Wahane S, Huang Y, et al. HDAC3 inhibition ameliorates spinal cord injury by immunomodulation. 2017;7:1–13. doi: 10.1038/s41598-017-08535-4
- Zhao Y, Mu H, Huang Y, et al. Microglia-specific deletion of histone deacetylase 3 promotes inflammation resolution, white matter integrity, and functional recovery in a mouse model of traumatic brain injury. J Neuroinflammation. 2022;19(1):201. doi: 10.1186/s12974-022-02563-2
- Wahane S, Zhou X, Zhou X, et al. Diversified transcriptional responses of myeloid and glial cells in spinal cord injury shaped by HDAC3 activity. Sci Adv. 2021;7(9):8811–8837. doi: 10.1126/sciadv.abd8811
- Mcquown SC, Wood MA. HDAC3 and the molecular brake pad hypothesis. Neurobiology of learning and memory. 2011;96:27–34. doi: 10.1016/j.nlm.2011.04.005
- Ishii S. The role of histone deacetylase 3 complex in nuclear hormone receptor action. Int J Mol Sci. 2021. [Accessed: 2021];22. doi: 10.3390/ijms22179138.
- Henn A, Lund S, Hedtjärn M, et al. The suitability of BV2 cells as alternative model system for primary microglia cultures or for animal experiments examining brain inflammation. ALTEX. 2009;26:83–94. doi: 10.14573/altex.2009.2.83
- Pollock TB, Cholico GN, Isho NF, et al. Transcriptome analyses in BV2 microglial cells following treatment with amino-terminal fragments of apolipoprotein E. Front Aging Neurosci. 2020;12:1–15. doi: 10.3389/fnagi.2020.00256
- Kacimi R, Giffard RG, Yenari MA. Endotoxin-activated microglia injure brain derived endothelial cells via NF-κB, JAK-STAT and JNK stress kinase pathways. J Inflamm. 2011;8(1):7. doi: 10.1186/1476-9255-8-7
- Marks PA. Discovery and development of SAHA as an anticancer agent. Oncogene. 2007;26(9):1351–1356. doi: 10.1038/sj.onc.1210204
- Malvaez M, McQuown SC, Rogge GA, et al. HDAC3-selective inhibitor enhances extinction of cocaine-seeking behavior in a persistent manner. Proceedings of the National Acadamy of Sciences of the United States of America. 2013;110:2647–2652. doi: 10.1073/pnas.121336411
- Furumai R, Matsuyama A, Kobashi N, et al. FK228 (depsipeptide) as a natural prodrug that inhibits class I histone deacetylases. Cancer Res. 2002;62(17):4916–4921.
- Maksoud MJE, Tellios V, An D, et al. Nitric oxide upregulates microglia phagocytosis and increases transient receptor potential vanilloid type 2 channel expression on the plasma membrane. Glia. 2019;67(12):2294–2311. doi: 10.1002/glia.23685
- Cherry JD, Olschowka JA, O’Banion MK. Neuroinflammation and M2 microglia: the good, the bad, and the inflamed. J Neuroinflammation. 2014;11(1):1–15. doi: 10.1186/1742-2094-11-98
- Yang Z, Ming XF. Functions of arginase isoforms in macrophage inflammatory responses: impact on cardiovascular diseases and metabolic disorders. Front Immunol. 2014;5:1–10. doi: 10.3389/fimmu.2014.00533
- Palmieri EM, McGinity C, Wink DA, et al. Nitric Oxide in macrophage immunometabolism: hiding in plain sight. Metabolites. 2020;10(11):429. doi: 10.3390/metabo10110429
- Schairer DO, Chouake JS, Nosanchuk JD, et al. The potential of nitric oxide releasing therapies as antimicrobial agents. Virulence. 2012;3:271–279.
- Figarella K, Uzcategui NL, Mogk S, et al. Morphological changes, nitric oxide production, and phagocytosis are triggered in vitro in microglia by bloodstream forms of Trypanosoma brucei. Sci Rep. 2018;8(1):15002. doi: 10.1038/s41598-018-33395-x
- Quintas C, Pinho D, Pereira C, et al. Microglia P2Y6 receptors mediate nitric oxide release and astrocyte apoptosis. J Neuroinflammation. 2014;11(1):141. doi: 10.1186/s12974-014-0141-3
- Arimoto T, Bing G. Up-regulation of inducible nitric oxide synthase in the substantia nigra by lipopolysaccharide causes microglial activation and neurodegeneration. Neurobiol Dis. 2003;12(1):35–45. doi: 10.1016/S0969-9961(02)00017-7
- Schell JB, Crane CA, Smith MF, et al. Differential ex vivo nitric oxide production by acutely isolated neonatal and adult microglia. J Neuroimmunol. 2007;189(1–2):75–87. doi: 10.1016/j.jneuroim.2007.07.004
- Collmann FM, Pijnenburg R, Hamzei-Taj S, et al. Individual in vivo profiles of microglia polarization after stroke, represented by the genes iNOS and Ym1. frontiers in immunology [online serial]. Front Immunol. 2019. [Accessed April 18, 2023]; 10. doi: 10.3389/fimmu.2019.01236
- Dibaj P, Nadrigny F, Steffens H, et al. NO mediates microglial response to acute spinal cord injury under ATP control in vivo. Glia. 2010;58(9):1133–1144. doi: 10.1002/glia.20993
- Yuste JE, Tarragon E, Campuzano CM, et al. Implications of glial nitric oxide in neurodegenerative diseases. Frontiers In Cellular Neuroscience [Online Serial]. 2015. [Accessed April 17, 2023];9. Accessed at https://www.frontiersin.org/articles/10.3389/fncel.2015.00322
- Cunningham C, Wilcockson DC, Campion S, et al. Central and systemic endotoxin challenges exacerbate the local inflammatory response and increase neuronal death during chronic neurodegeneration. J Neurosci. 2005;25(40):9275–9284. doi: 10.1523/JNEUROSCI.2614-05.2005
- Scheiblich H, Roloff F, Singh V, et al. Nitric oxide/cyclic GMP signaling regulates motility of a microglial cell line and primary microglia in vitro. Brain Res. 2014;1564:9–21. doi: 10.1016/j.brainres.2014.03.048
- Jun CD, Han MK, Kim UH, et al. Nitric oxide induces ADP-ribosylation of actin in murine macrophages: association with the inhibition of pseudopodia formation, phagocytic activity, and adherence on a laminin substratum. Cell Immunol. 1996;174(1):25–34. doi: 10.1006/cimm.1996.0290
- Kopec KK, Carroll RT. Phagocytosis is regulated by nitric oxide in murine microglia. Nitric Oxide. 2000;4(2):103–111. doi: 10.1006/niox.2000.0280
- Kakita H, Aoyama M, Nagaya Y, et al. Diclofenac enhances proinflammatory cytokine-induced phagocytosis of cultured microglia via nitric oxide production. Toxicol Appl Pharmacol. 2013;268(2):99–105. doi: 10.1016/j.taap.2013.01.024
- Scheiblich H, Bicker G. Nitric oxide regulates antagonistically phagocytic and neurite outgrowth inhibiting capacities of microglia. Devel Neurobio. 2016;76(5):566–584. doi: 10.1002/dneu.22333
- Fu R, Shen Q, Xu P, et al. Phagocytosis of microglia in the central nervous system diseases. Mol Neurobiol. 2014;49(3):1422–1434. doi: 10.1007/s12035-013-8620-6
- Jordan P, Costa A, Specker E, et al. Small molecule inhibiting microglial nitric oxide release could become apotential treatment for neuroinflammation. PLOS ONE. 2023;18:e0278325. doi: 10.1371/journal.pone.0278325
- Zhang Z-Y, Schluesener HJ. Oral Administration of histone deacetylase inhibitor MS-275 ameliorates neuroinflammation and cerebral amyloidosis and improves behavior in a mouse model. J Neuropathol Exp Neurol. 2013;72(3):178–185. doi: 10.1097/NEN.0b013e318283114a
- Mullican SE, Gaddis CA, Alenghat T, et al. Histone deacetylase 3 is an epigenomic brake in macrophage alternative activation. Genes Dev. 2011;25(23):2480–2488. doi: 10.1101/gad.175950.111
- Ghiboub M, Zhao J, Li Yim AYF, et al. HDAC3 mediates the inflammatory response and LPS tolerance in human monocytes and macrophages. Front Immunol. 2020;11:2608. doi:10.3389/fimmu.2020.550769
- Chen X, Barozzi I, Termanini A, et al. Requirement for the histone deacetylase Hdac3 for the inflammatory gene expression program in macrophages. PNAS. 2012;109:E2865–E2874. doi: 10.1073/pnas.1121131109
- Nguyen HCB, Adlanmerini M, Hauck AK, et al. Dichotomous engagement of HDAC3 activity governs inflammatory responses. Nature Research. 2020;584(7820):286–290. doi: 10.1038/s41586-020-2576-2
- Grégoire S, Xiao L, Nie J, et al. Histone deacetylase 3 interacts with and deacetylates myocyte enhancer factor 2. molecular and cellular biology. Mol Cell Biol. 2007;27(4):1280–1295. doi: 10.1128/MCB.00882-06
- Chuang HC, Chang CW, Chang GD, et al. Histone deacetylase 3 binds to and regulates the GCMa transcription factor. Nucleic Acids Research. 2006;34:1459. doi: 10.1093/nar/gkl048
- Chen LF, Fischle W, Verdin E, et al. Duration of nuclear NF-κB action regulated by reversible acetylation. Sci. 2001;293(5535):1653–1657. doi: 10.1126/science.1062374
- Yang L, Chen S, Zhao Q, et al. Histone deacetylase 3 contributes to the antiviral innate immunity of macrophages by interacting with FOXK1 to regulate STAT1/2 transcription. Cell Rep. 2022;38(4):110302. doi: 10.1016/j.celrep.2022.110302
- Bennett FC, Bennett ML, Yaqoob F, et al. A combination of ontogeny and CNS environment establishes microglial identity. Neuron. 2018;98(6):1170–1183.e8. doi: 10.1016/j.neuron.2018.05.014