The Effect of Morphine on REST Expression in Human Neuroblastoma NMB Cells.
- Author:
Do Kyung KIM
1
;
Chun Sung KIM
;
Heung Joong KIM
;
Joong Ki KOOK
;
Seung Hee KIM
;
Baek Hee LEE
;
Yun Ho LEE
;
Shin Yeob MO
;
Horace H LOH
Author Information
1. Oral Biology Research Institute, Chosun University School of Dentistry, Gwangju 501-759, Korea. kdk@chosun.ac.kr
- Publication Type:Original Article
- Keywords:
morphine;
REST;
mu opioid receptors;
neuroblastoma cells
- MeSH:
Analgesics;
Blotting, Western;
Humans;
Morphine;
Neuroblastoma;
Neurons;
Receptors, Opioid, mu;
RNA, Messenger;
Somatostatin;
Transcription Factors
- From:International Journal of Oral Biology
2010;35(2):69-74
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
The mu opioid receptor (MOR) has been regarded as the main site of interaction with analgesics in major clinical use, particularly morphine. The repressor element-1 silencing transcription factor (REST) functions as a transcriptional repressor of neuronal genes in non-neuronal cells. However, it is expressed in certain mature neurons, suggesting that it may have complex and novel roles. In addition, the interactions between MOR and REST and their functions remain unclear. In this study, we examined the effects of morphine on the expression of REST mRNA and protein in human neuroblastoma NMB cells to investigate the roles of REST induced by MOR activation in neuronal cells. To determine the effects of morphine on REST expression, we performed RT-PCR, real-time quantitative RT-PCR, western blot analysis and radioligand binding assays in NMB cells. By RT-PCR and real-time quantitative RT-PCR, the expression of REST was found to be unchanged by either the MOR agonist morphine or the MOR specific antagonist CTOP. By western blot, morphine was shown to significantly inhibit the expression of REST, but this suppression was completely blocked by treatment with CTOP. In the radioligand binding assay, the overexpression of REST led to an increased opioid ligand binding activity of endogenous MOR in the NMB cells. These results together suggest that morphine inhibits the expression of REST in human neuroblastoma cells through a post-transcriptional regulatory mechanism mediated through MOR.
