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Updated: Aug 27, 2025
An Experimental Paradigm for the Prediction of Post-Operative Pain PPOP
Published on: January 27, 2010
Perioperative stress prolong post-surgical pain via miR-339-5p targeting oprm1 in the amygdala
1Department of Anesthesiology, General Hospital of The Southern Theater Command of PLA, Guangzhou, China.
Background:
The decreased expression of mu-opioid receptors (MOR) in the amygdala may be a key molecular in chronic post-surgical pain (CPSP). It is known that miR-339-5p expression in the amygdala of a stressed rat model was increased. Analyzed by RNAhybrid, miR-339-5p could target opioid receptor mu 1 (oprm1) which codes MOR directly. So, the authors hypothesized that miR-339-5p could regulate the expression of MOR via targeting oprm1 and cause the effects to CPSP.
Methods:
To simulate perioperative short-term stress, a perioperative stress prolongs incision-induced pain hypersensitivity without changing basal pain perception rat model was built. A pmiR-RB-REPORT™ dual luciferase assay was taken to verify whether miR-339-5p could act on oprm1 as a target. The serum glucocorticoid level of rats was test. Differential expressions of MOR, GFAP, and pERK1/2 in each group of the rats' amygdala were tested, and the expressions of miR-339-5p in each group of rats' amygdalas were also measured.
Results:
Perioperative stress prolonged the recovery time of incision pain. The expression of MOR was down-regulated in the amygdala of rats in stress + incision (S + IN) group significantly compared with other groups (P < 0.050). miR-339-5p was up-regulated in the amygdala of rats in group S + IN significantly compared with other groups (P < 0.050). miR-339-5p acts on oprm1 3'UTR and take MOR mRNA as a target.
Conclusions:
Perioperative stress could increase the expression of miR-339-5p, and miR-339-5p could cause the expression of MOR to decrease via targeting oprm1. This regulatory pathway maybe an important molecular mechanism of CPSP.
Insights
Perioperative stress increases miR-339-5p, which targets the opioid receptor mu 1 (oprm1) gene. This down-regulates mu-opioid receptors (MOR) in the amygdala, potentially causing chronic post-surgical pain (CPSP).
Area of Science:
- Neuroscience
- Molecular Biology
- Pain Research
Background:
- Decreased mu-opioid receptor (MOR) expression in the amygdala is linked to chronic post-surgical pain (CPSP).
- miR-339-5p expression is elevated in the amygdala of stressed rats.
- Bioinformatic analysis suggests miR-339-5p targets the opioid receptor mu 1 (oprm1) gene, which encodes MOR.
Purpose of the Study:
- To investigate the role of miR-339-5p in regulating MOR expression.
- To determine if miR-339-5p contributes to chronic post-surgical pain (CPSP) mechanisms.
- To validate the targeting of oprm1 by miR-339-5p.
Main Methods:
- A rat model simulating perioperative stress and incision-induced pain was established.
- Dual luciferase assay was used to confirm miR-339-5p targeting of oprm1.
- Expression levels of MOR, miR-339-5p, GFAP, and pERK1/2 in the amygdala were quantified.
Main Results:
- Perioperative stress prolonged pain hypersensitivity and reduced MOR expression in the amygdala.
- miR-339-5p expression was significantly upregulated in stressed rats with incision.
- miR-339-5p was confirmed to target the 3'UTR of oprm1, reducing MOR mRNA levels.
Conclusions:
- Perioperative stress elevates miR-339-5p, leading to decreased MOR expression via oprm1 targeting.
- This miR-339-5p/oprm1/MOR pathway is a potential molecular mechanism underlying CPSP.
- Findings highlight a novel regulatory mechanism in the development of chronic pain.
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