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Increased miR-132-3p expression is associated with chronic neuropathic pain
M Leinders1, N Üçeyler2, R A Pritchard3
1Department of Neurology, University of Würzburg, Würzburg, Germany; Department of Anesthesiology, University of California, San Diego, La Jolla, CA 92093, USA.
Experimental Neurology
|June 29, 2016
Summary
MicroRNA-132-3p (miR-132-3p) is elevated in patients with neuropathic pain. Inhibiting miR-132-3p in rats reduced pain, while enhancing it induced pain, indicating a pro-nociceptive role.
Area of Science:
- Neuroscience
- Immunology
- Molecular Biology
Background:
- Neuro-immune imbalance is key in chronic neuropathic pain.
- MicroRNAs (miRNAs) regulate neuronal and immune functions, potentially driving pain.
- The role of miR-132-3p in neuropathic pain requires investigation.
Purpose of the Study:
- To investigate the role of miR-132-3p in human neuropathic pain patients.
- To analyze miR-132-3p expression and function in an animal model of neuropathic pain.
Main Methods:
- Measured miR-132-3p levels in white blood cells and sural nerve biopsies from neuropathy patients and controls.
- Assessed miR-132-3p expression in rat dorsal root ganglia and spinal cord after spared nerve injury (SNI).
- Modulated miR-132-3p using antagonists and mimetics in rats and evaluated pain behaviors.
Main Results:
- miR-132-3p was significantly increased in white blood cells of neuropathy patients (2.6-fold).
- Sural nerve biopsies showed a slight miR-132-3p upregulation in painful neuropathies (1.2-fold).
- Spinal miR-132-3p levels peaked during established allodynia in SNI rats; antagonists reversed allodynia, while mimetics induced pain.
Conclusions:
- miR-132-3p is upregulated in neuropathic pain conditions.
- miR-132-3p acts as a pro-nociceptive factor in chronic neuropathic pain.
- Targeting miR-132-3p may offer a therapeutic strategy for neuropathic pain.

