Related Experiment Video
Updated: Aug 6, 2025
Intracerebroventricular Treatment with Resiniferatoxin and Pain Tests in Mice
Published on: September 2, 2020
Intradermal miR-16-5p targets Akt3 and reduces RTX-induced postherpetic neuralgia-mimic pain in mice
Dexin Zhang1, Lulin Ma2, Xinran Tan1
1Department of Anesthesiology, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou, China; Department of Pain Medicine, Affiliated Hospital of Zunyi Medical University, Zunyi, Guizhou, China.
Abstract:
The molecular mechanisms of refractory pain in postherpetic neuralgia (PHN) patients are not fully understood. PHN may be related to skin abnormality after herpes zoster induced skin lesions. We previously reported 317 differentially expressed microRNAs (miRNAs) in PHN skin compared with the contralateral normal mirror skin. In this study, 19 differential miRNAs were selected and the expression was validated in other 12 PHN patients. The expression levels of miR-16-5p, miR-20a-5p, miR-505-5p, miR-3664-3p, miR-4714-3p and let-7a-5p are lower in PHN skin, which is the same as those in microarray experiment. To evaluate the effects of cutaneous miRNA on PHN, the expression of candidate miRNAs is further observed in resiniferatoxin (RTX) induced PHN-mimic mice model. In the plantar skin of RTX mice, miR-16-5p and let-7a-5p are downregulated, with the same expression trend of PHN patients. In addition, intraplantar injection of agomir-16-5p reduced mechanical hyperalgesia, and improved thermal hypoalgesia in RTX mice. Furthermore, agomir-16-5p down-regulated the expression levels of Akt3, which is the target gene of agomir-16-5p. These results suggest that intraplantar miR-16-5p may alleviate RTX induced PHN-mimic pain by inhibiting the expression of Akt3 in the skin.
Insights
MicroRNA-16-5p (miR-16-5p) may alleviate postherpetic neuralgia (PHN) pain. Topical application of miR-16-5p reduced pain sensitivity in a mouse model by inhibiting the Akt3 gene.
Area of Science:
- Molecular Biology
- Neuroscience
- Dermatology
Background:
- Postherpetic neuralgia (PHN) pain mechanisms remain unclear, potentially linked to skin abnormalities post-herpes zoster.
- Previous research identified 317 differentially expressed microRNAs (miRNAs) in PHN skin.
- This study validates specific miRNA expression changes in PHN patients and a mouse model.
Purpose of the Study:
- To investigate the role of cutaneous microRNAs in refractory pain associated with PHN.
- To validate the expression levels of specific miRNAs in PHN patients and a PHN-mimic mouse model.
- To explore the therapeutic potential of miR-16-5p in alleviating PHN-like pain.
Main Methods:
- Validated expression of 19 differential miRNAs in skin samples from 12 PHN patients.
- Assessed candidate miRNA expression in a resiniferatoxin (RTX)-induced PHN-mimic mouse model.
- Administered agomir-16-5p (miR-16-5p mimic) intraplantarly in RTX mice and analyzed Akt3 expression.
Main Results:
- miR-16-5p and let-7a-5p were downregulated in PHN skin and RTX-induced mouse models.
- Intraplantar agomir-16-5p reduced mechanical hyperalgesia and improved thermal hypoalgesia in RTX mice.
- Agomir-16-5p treatment led to decreased expression of its target gene, Akt3.
Conclusions:
- Cutaneous miR-16-5p downregulation is associated with PHN.
- Intraplantar miR-16-5p delivery shows potential for alleviating PHN-like pain.
- miR-16-5p may exert its analgesic effect by inhibiting Akt3 expression in the skin.
