ArticleMolecular pharmacology2010
Up-regulation of the mu-opioid receptor gene is mediated through chromatin remodeling and transcriptional factors in differentiated neuronal cells.
Article in Molecular pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 51 citations in OpenAlex.
- OPRM1 Methylation Contributes to Opioid Tolerance in Cancer Patients.The journal of pain · 2017Trial
- MeCP2 functions as a DNA methylation reader in immune homeostasis and cancer.Frontiers in epigenetics and epigenomics · 2026Review
- Lactobacillus rhamnosus GG and butyrate supplementation in rats with bone cancer reduces mechanical allodynia and increases expression of μ-opioid receptor in the spinal cord.Frontiers in molecular neuroscience · 2023Article
- Epigenetic Alterations in Prescription Opioid Misuse: New Strategies for Precision Pain Management.Genes · 2021Review
- Synergism of Proneurogenic miRNAs Provides a More Effective Strategy to Target Glioma Stem Cells.Cancers · 2021Article
- Fentanyl Inhibits Air Puff-Evoked Sensory Information Processing in Mouse Cerebellar Neurons RecordedFrontiers in systems neuroscience · 2020Article
- The Mechanisms Involved in Morphine Addiction: An Overview.International journal of molecular sciences · 2019Review
- Molecular Genetics and New Medication Strategies for Opioid Addiction.The American journal of psychiatry · 2018Review
- Histone deacetylase 2 is involved in µ‑opioid receptor suppression in the spinal dorsal horn in a rat model of chronic pancreatitis pain.Molecular medicine reports · 2018Article
- mPer1 promotes morphine-induced locomotor sensitization and conditioned place preference via histone deacetylase activity.Psychopharmacology · 2017Article
- Epigenetic Activation ofMolecular pharmacology · 2017Article
- H4K5 histone acetylation ofExperimental and therapeutic medicine · 2016Article
- 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
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- Litter and sex effects on maternal behavior and DNA methylation of the Nr3c1 exon 17 promoter gene in hippocampus and cerebellum.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2014Article
- Epigenetics: a promising paradigm for better understanding and managing pain.The journal of pain · 2013Review
- Inhibition of c-Jun NH2-terminal kinase stimulates mu opioid receptor expression via p38 MAPK-mediated nuclear NF-κB activation in neuronal and non-neuronal cells.Biochimica et biophysica acta · 2013Article
- 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
- Dietary methyl content regulates opioid responses in mice.Journal of pain research · 2013Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
The effects of morphine are mediated mainly through the mu opioid receptor (MOR). Expression of the MOR is up-regulated during neuronal differentiation in P19 embryonal carcinoma cells and epigenetic changes play an important role in MOR up-regulation. This study investigates the basis for differentiation-dependent alterations of MOR chromatin by studying the recruitment or dissociation of several factors to the remodeled chromatin locus. Chromatin immunoprecipitation assays were used to demonstrate the recruitment of the transcriptional activator Sp1 and the chromatin remodeling factors Brg1 and BAF155 to this promoter, as well as the dissociation of repressors [histone deacetylases, mSin3A, Brm, and methyl-CpG-binding protein 2 (MeCP2)]. Histone modifications (acetylation, induction of histone H3-lys4 methylation, and reduction of H3-lys9 methylation) were consistently detected on this promoter. Overexpression of Sp1 strongly enhanced MOR promoter activity, and the histone deacetylase inhibitor trichostatin A also increased promoter activity. In vitro DNA CpG-methylation of the promoter partially blocked binding of the Sp1 factor but induced MeCP2 binding. Coimmunoprecipitation studies also found novel evidence of an endogenous MeCP2 interaction with Sp3 but a weaker interaction with Sp1. Overall, the results suggest that during neuronal differentiation, MeCP2 and DNA methylation mediate remodeling of the MOR promoter by chromatin remodeling factors (Brg1 and BAF155) from a compacted state to a conformation allowing access for transcriptional factors. Subsequent recruitment of the activating transcription factor Sp1 to the remodeled promoter results in MOR up-regulation.
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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.