ArticleJournal of cellular and molecular medicine2009
Epigenetic programming of mu-opioid receptor gene in mouse brain is regulated by MeCP2 and Brg1 chromatin remodelling factor.
Article in Journal of cellular and molecular medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
37 citing papers in PubMed, 65 citations in OpenAlex.
- Epigenetic mechanisms of HIV and opioid-induced neuropathology: Potential therapies and interventions.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Mechanisms Underlying Mu Opioid Receptor Effects on Parallel Fiber-Purkinje Cell Synaptic Transmission in Mouse Cerebellar Cortex.Frontiers in synaptic neuroscience · 2022Article
- The aetiology of social deficits within mental health disorders: The role of the immune system and endogenous opioids.Brain, behavior, & immunity - health · 2020Review
- Sex-Based Mhrt Methylation Chromatinizes MeCP2 in the Heart.iScience · 2019Article
- Sex differences in neural mechanisms mediating reward and addiction.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019Review
- Epigenetic Activation ofMolecular pharmacology · 2017Article
- Post-Transcriptional Regulation of the Human Mu-Opioid Receptor (MOR) by Morphine-Induced RNA Binding Proteins hnRNP K and PCBP1.Journal of cellular physiology · 2017Article
- A case-controlled comparison of postoperative analgesic dosing between girls with Rett syndrome and girls with and without developmental disability undergoing spinal fusion surgery.Paediatric anaesthesia · 2017Article
- Article
- DNA methylation at the mu-1 opioid receptor gene (Pharmacogenomics and personalized medicine · 2017Article
- H4K5 histone acetylation ofExperimental and therapeutic medicine · 2016Article
- Pain experience and expression in Rett syndrome: Subjective and objective measurement approaches.Journal of developmental and physical disabilities · 2015Article
- Stabilization of morphine tolerance with long-term dosing: association with selective upregulation of mu-opioid receptor splice variant mRNAs.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Epigenetic regulation of persistent pain.Translational research : the journal of laboratory and clinical medicine · 2015Review
- Epigenetic signaling in psychiatric disorders.Journal of molecular biology · 2014Review
- Increased methylation of the MOR gene proximal promoter in primary sensory neurons plays a crucial role in the decreased analgesic effect of opioids in neuropathic pain.Molecular pain · 2014Article
- Epigenetic mechanisms of drug addiction.Neuropharmacology · 2014Review
- Epigenetics, drugs of abuse, and the retroviral promoter.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2013Review
- Epigenetics: a promising paradigm for better understanding and managing pain.The journal of pain · 2013Review
- MicroRNA 339 down-regulates μ-opioid receptor at the post-transcriptional level in response to opioid treatment.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
The pharmacological action of morphine as a pain medication is mediated primarily through the mu-opioid receptor (MOR). With few exceptions, MOR is expressed in brain regions where opioid actions take place. The basis for this unique spatial expression of MOR remains undetermined. Recently, we reported that DNA methylation of the MOR promoter plays an important role in regulating MOR in P19 cells. In this study, we show that the differential expression of MOR in microdissected mouse brain regions coincides with DNA methylation and histone modifications. MOR expression could be induced by a demethylating agent or a histone deacetylase inhibitor in MOR-negative cells, suggesting that the MOR gene can be silenced under epigenetic control. Increases in the in vivo interaction of methyl-CpG-binding protein 2 (MeCP2) were observed in the cerebellum, in which the MOR promoter was hypermethylated and MOR expression was the lowest among all brain regions tested. MeCP2 is associated closely with Rett syndrome, a neurodevelopmental disorder. We also established novel evidence for a functional role for MeCP2's association with the chromatin-remodelling factor Brg1 and DNA methyltransferase Dnmt1, suggesting a possible role for MeCP2 in chromatin remodelling during MOR gene regulation. We conclude that MOR gene expression is epigenetically programmed in various brain regions and that MeCP2 assists the epigenetic program during DNA methylation and chromatin remodelling of the MOR promoter.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.