The role of transcription factors Sp1 and YY1 in proximal promoter region in initiation of transcription of the mu opioid receptor gene in human lymphocytes

2008 ◽  
Vol 104 (1) ◽  
pp. 237-250 ◽  
Author(s):  
Hui Li ◽  
Han Liu ◽  
Zimei Wang ◽  
Xinhua Liu ◽  
Liyuan Guo ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Opioid Receptor ◽  
Promoter Region ◽  
Receptor Gene ◽  
Human Lymphocytes ◽  
Mu Opioid Receptor ◽  
Proximal Promoter ◽  
Mu Opioid ◽  
Initiation Of Transcription

scholarly journals The Role of the Asn40Asp Polymorphism of the Mu Opioid Receptor Gene (OPRM1) on Alcoholism Etiology and Treatment: A Critical Review

2011 ◽  
Vol 36 (3) ◽  
pp. 385-394 ◽  
Author(s):  
Lara A. Ray ◽  
Christina S. Barr ◽  
Julie A. Blendy ◽  
David Oslin ◽  
David Goldman ◽  
...  
Keyword(s):  
Opioid Receptor ◽  
Critical Review ◽  
Receptor Gene ◽  
Mu Opioid Receptor ◽  
Mu Opioid

scholarly journals Evidence of Endogenous Mu Opioid Receptor Regulation by Epigenetic Control of the Promoters

2007 ◽  
Vol 27 (13) ◽  
pp. 4720-4736 ◽  
Author(s):  
Cheol Kyu Hwang ◽  
Kyu Young Song ◽  
Chun Sung Kim ◽  
Hack Sun Choi ◽  
Xiao-Hong Guo ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Opioid Receptor ◽  
Promoter Region ◽  
Histone Deacetylase Inhibitors ◽  
Mu Opioid Receptor ◽  
Histone Deacetylation ◽  
Epigenetic Mechanism ◽  
Proximal Promoter ◽  
Mu Opioid

ABSTRACT The pharmacological effect of morphine as a painkiller is mediated mainly via the mu opioid receptor (MOR) and is dependent on the number of MORs in the cell surface membrane. While several studies have reported that the MOR gene is regulated by various cis- and trans-acting factors, many questions remain unanswered regarding in vivo regulation. The present study shows that epigenetic silencing and activation of the MOR gene are achieved through coordinated regulation at both the histone and DNA levels. In P19 mouse embryonal carcinoma cells, expression of the MOR was greatly increased after neuronal differentiation. MOR expression could also be induced by a demethylating agent (5′-aza-2′-deoxycytidine) or histone deacetylase inhibitors in the P19 cells, suggesting involvement of DNA methylation and histone deacetylation for MOR gene silencing. Analysis of CpG DNA methylation revealed that the proximal promoter region was unmethylated in differentiated cells compared to its hypermethylation in undifferentiated cells. In contrast, the methylation of other regions was not changed in either cell type. Similar methylation patterns were observed in the mouse brain. In vitro methylation of the MOR promoters suppressed promoter activity in the reporter assay. Upon differentiation, the in vivo interaction of MeCP2 was reduced in the MOR promoter region, coincident with histone modifications that are relevant to active transcription. When MeCP2 was disrupted using MeCP2 small interfering RNA, the endogenous MOR gene was increased. These data suggest that DNA methylation is closely linked to the MeCP2-mediated chromatin structure of the MOR gene. Here, we propose that an epigenetic mechanism consisting of DNA methylation and chromatin modification underlies the cell stage-specific mechanism of MOR gene expression.

scholarly journals Variation of the human mu-opioid receptor (OPRM1) gene predicts vulnerability to frustration

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Alan M. Daniel ◽  
Brenda G. Rushing ◽  
Karla Y. Tapia Menchaca
Keyword(s):  
Individual Differences ◽  
Animal Models ◽  
Opioid Receptor ◽  
Receptor Gene ◽  
Emotional Reaction ◽  
Mu Opioid Receptor ◽  
Reward Processing ◽  
Physical Pain ◽  
Mu Opioid ◽  
Allelic Differences

AbstractUnderstanding the emotional reaction to loss, or frustration, is a critical problem for the field of mental health. Animal models of loss have pointed to the opioid system as a nexus of frustration, physical pain, and substance abuse. However, few attempts have been made to connect the results of animal models of loss to human behavior. Allelic differences in the human mu opioid receptor gene, notably the A118G single nucleotide polymorphism, have been linked to individual differences in pain sensitivity, depressive symptoms, and reward processing. The present study explored the relationship between A118G and behavior in two frustrating tasks in humans. Results showed that carriers of the mutant G-allele were slower to recover behavior following a reward downshift and abandoned a frustrating task earlier than those without the mutation. Additionally, G-carriers were more sensitive to physical pain. These results highlight the overlap between frustration and pain, and suggest that genetic variation in opioid tone may contribute to individual differences in vulnerability and resilience following emotional disturbances.

A118G Single Nucleotide Polymorphism of Human μ-Opioid Receptor Gene Influences Pain Perception and Patient-controlled Intravenous Morphine Consumption after Intrathecal Morphine for Postcesarean Analgesia

2008 ◽  
Vol 109 (3) ◽  
pp. 520-526 ◽  
Author(s):  
Alex T. Sia ◽  
Yvonne Lim ◽  
Eileen C. P. Lim ◽  
Rachelle W. C. Goh ◽  
Hai Yang Law ◽  
...  
Keyword(s):  
Opioid Receptor ◽  
Pain Perception ◽  
Intrathecal Morphine ◽  
Receptor Gene ◽  
Mu Opioid Receptor ◽  
Morphine Consumption ◽  
Mu Opioid ◽  
Pain Scores ◽  
Significant Difference ◽  
Intravenous Morphine

Background Previous studies have shown that genetic variability at position 118 of the human mu-opioid receptor gene altered patients' response to intravenous morphine. The purpose of this study was to investigate whether this polymorphism contributes to the variability in response to morphine for postcesarean analgesia. Methods After investigators obtained informed consent, 588 healthy women received 0.1 mg intrathecal morphine for postcesarean analgesia. Their blood samples were genotyped for the A118G polymorphism-A118 homozygous (AA), heterozygous (AG), or homozygous for the G allele (GG). Pain scores, the severity of nausea and vomiting, the incidence of pruritus, and the total self-administered intravenous morphine were recorded for the first 24 postoperative hours. Results Two hundred seventy women (46%) were AA, 234 (40%) were AG, and 82 (14%) were GG. The 24-h self-administered intravenous morphine consumption was lowest in the AA group (P = 0.001; mean, 5.9; 95% confidence interval, 5.1-6.8) versus the AG (8.0; 6.9-9.1) and GG groups (9.4; 7.3-11.5). Pain scores were lowest in the AA group and highest in the GG group, with a statistically significant difference detected between AA, AG, and GG (P = 0.049). Total morphine consumption was also influenced by patients' age and paying status. AA group was associated with the highest incidence of nausea (26 of 272 [9.6%]; P = 0.02) versus the other two groups (13 of 234 [5.6%] and 1 of 82 [1.2%] for AG and GG, respectively). Conclusion Genetic variation at position 118 of the mu-opioid receptor is associated with interindividual differences in pain scores, self-administered intravenous morphine, and the incidence of nausea postoperatively.

scholarly journals Deciphering the Novel Role of Gαz in Mu Opioid Receptor Signaling

2021 ◽  
Vol 35 (S1) ◽  
Author(s):  
Miriam Barnett ◽  
Brian Knapp ◽  
Jean Bidlack
Keyword(s):  
Opioid Receptor ◽  
Mu Opioid Receptor ◽  
The Novel ◽  
Receptor Signaling ◽  
Mu Opioid

Mu Opioid Receptor Gene (OPRM1) in Patients With Opiate Use Disorder

2020 ◽  
Vol 19 (1) ◽  
pp. 16-21
Author(s):  
Nehal Mostafa ◽  
Maha W. Mobasher ◽  
Heba N. El Baz ◽  
Mohamed A. Khalil
Keyword(s):  
Opioid Receptor ◽  
Receptor Gene ◽  
Mu Opioid Receptor ◽  
Mu Opioid ◽  
Opiate Use ◽  
Opiate Use Disorder

scholarly journals Deletion of the mu opioid receptor gene in mice reshapes the reward–aversion connectome

2016 ◽  
Vol 113 (41) ◽  
pp. 11603-11608 ◽  
Author(s):  
Anna E. Mechling ◽  
Tanzil Arefin ◽  
Hsu-Lei Lee ◽  
Thomas Bienert ◽  
Marco Reisert ◽  
...  
Keyword(s):  
Functional Connectivity ◽  
Opioid Receptor ◽  
Resting State ◽  
Receptor Gene ◽  
Resting State Fmri ◽  
Mu Opioid Receptor ◽  
Major Influence ◽  
Mu Opioid ◽  
Brain Connectome ◽  
Intergroup Comparison

Connectome genetics seeks to uncover how genetic factors shape brain functional connectivity; however, the causal impact of a single gene’s activity on whole-brain networks remains unknown. We tested whether the sole targeted deletion of the mu opioid receptor gene (Oprm1) alters the brain connectome in living mice. Hypothesis-free analysis of combined resting-state fMRI diffusion tractography showed pronounced modifications of functional connectivity with only minor changes in structural pathways. Fine-grained resting-state fMRI mapping, graph theory, and intergroup comparison revealed Oprm1-specific hubs and captured a unique Oprm1 gene-to-network signature. Strongest perturbations occurred in connectional patterns of pain/aversion-related nodes, including the mu receptor-enriched habenula node. Our data demonstrate that the main receptor for morphine predominantly shapes the so-called reward/aversion circuitry, with major influence on negative affect centers.

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