Global hypomethylation defines a sub-population of reactive microglia/macrophages in experimental traumatic brain injury
- PMID: 17996371
- DOI: 10.1016/j.neulet.2007.09.061
Global hypomethylation defines a sub-population of reactive microglia/macrophages in experimental traumatic brain injury
Abstract
Global alterations in gene expression have been observed in different traumatic brain injury (TBI) models and are considered of crucial importance to the development of subsequent tissue injury and repair. Cytosine methylation is a well-known process of endogenous DNA modification in mammals and the primary mechanism responsible for changes in epigenetic gene expression. Here we have investigated the early global spatio-temporal changes of the status of cellular DNA methylation in a rat TBI model by immunohistochemistry and analyzed the effects of dexamethasone on these changes. Global cellular hypomethylation was seen as early as day 1 in pannecrosis and day 2 in peripannecrosis following TBI. A sub-population of reactive microglia/macrophages was identified as the major source of hypomethylated cells by double-staining experiments. Further, peripheral administration of dexamethasone suppressed this lesional hypomethylation at day 2 post-injury. In sum, our data suggest that lesional hypomethylation defines a sub-population of activated microglia/macrophages involved in the early processes following traumatic brain injury.
Similar articles
-
Lesional accumulation of CD163+ macrophages/microglia in rat traumatic brain injury.Brain Res. 2012 Jun 21;1461:102-10. doi: 10.1016/j.brainres.2012.04.038. Epub 2012 Apr 27. Brain Res. 2012. PMID: 22583855
-
From traumatic brain injury to posttraumatic epilepsy: what animal models tell us about the process and treatment options.Epilepsia. 2009 Feb;50 Suppl 2:21-9. doi: 10.1111/j.1528-1167.2008.02007.x. Epilepsia. 2009. PMID: 19187291 Review.
-
Early attenuation of lesional interleukin-16 up-regulation by dexamethasone and FTY720 in experimental traumatic brain injury.Neuropathol Appl Neurobiol. 2008 Jun;34(3):330-9. doi: 10.1111/j.1365-2990.2007.00893.x. Epub 2007 Nov 5. Neuropathol Appl Neurobiol. 2008. PMID: 17983426
-
Kinetics of the cellular immune response following closed head injury.Acta Neurochir (Wien). 2007 Mar;149(3):281-9. doi: 10.1007/s00701-006-1095-8. Epub 2007 Feb 9. Acta Neurochir (Wien). 2007. PMID: 17288002
-
Lesional accumulation of P2X4 receptor+ monocytes following experimental traumatic brain injury.Exp Neurol. 2006 Jan;197(1):252-7. doi: 10.1016/j.expneurol.2005.09.015. Epub 2005 Nov 2. Exp Neurol. 2006. PMID: 16259982
Cited by
-
Brain-Derived Neurotrophic Factor in Pediatric Acquired Brain Injury and Recovery.Biomolecules. 2024 Feb 4;14(2):191. doi: 10.3390/biom14020191. Biomolecules. 2024. PMID: 38397427 Free PMC article. Review.
-
Traumatic brain injury-associated epigenetic changes and the risk for neurodegenerative diseases.Front Neurosci. 2023 Sep 19;17:1259405. doi: 10.3389/fnins.2023.1259405. eCollection 2023. Front Neurosci. 2023. PMID: 37795186 Free PMC article.
-
Reduced non-CpG methylation is a potential epigenetic target after spinal cord injury.Neural Regen Res. 2023 Nov;18(11):2489-2496. doi: 10.4103/1673-5374.371399. Neural Regen Res. 2023. PMID: 37282481 Free PMC article.
-
Epigenetic and epitranscriptomic regulation of axon regeneration.Mol Psychiatry. 2023 Apr;28(4):1440-1450. doi: 10.1038/s41380-023-02028-9. Epub 2023 Mar 15. Mol Psychiatry. 2023. PMID: 36922674 Free PMC article. Review.
-
Epigenetic Alterations in Sports-Related Injuries.Genes (Basel). 2022 Aug 17;13(8):1471. doi: 10.3390/genes13081471. Genes (Basel). 2022. PMID: 36011382 Free PMC article. Review.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
