PuSH - Publikationsserver des Helmholtz Zentrums München: PRMT2-mediated upregulation of miR-323-3p in sensory neurons promotes trigeminal neuropathic pain by targeting Kv2.1 channels.

Informationen

Hinweise zu Qualitätskriterien von Zeitschriften

Open-Access-Richtlinie der Helmholtz-Gemeinschaft 2016

CC Licencences

Metriken für Publikationen

Navigation

Startseite

English

EVA: Veröffentlichen

Neuer EVA Antrag

Recherche

Erweiterte Suche

Durchblättern nach ...

... HMGU-Autoren/Konsortien

... Organisationsstruktur

... Zeitschriften

... Publikationstypen

... Forschungsdaten

... Arbeitsgruppen

... Erscheinungsjahr

Publikationen im Überblick

Statistik

HGF Fortschrittsbericht

OA Publikationen

Eintragen

Neue Publikation eintragen

Neue Publikation holen aus...

...EVA

Fehlende Publikation melden

Highlights

Suche

Hilfe & Kontakt

Ansprechpartner

Hilfe

Datenschutz

Helmholtz Open Science

Bibliometrische Indikatoren

SHERPA/RoMEO

DOAJ

Export:

Text

Endnote (RIS) BIB

BibTeX

Qi, R.* ; Tao, Y.* ; Wang, S.* ; Zhou, Y.* ; Sun, Y.* ; Jiang, D. ; Huang, Z.* ; Chen, G.* ; Zhao, G.* ; Zhang, Y.* ; Rui, Y.* ; Tao, J.*

PRMT2-mediated upregulation of miR-323-3p in sensory neurons promotes trigeminal neuropathic pain by targeting Kv2.1 channels.

Cell Rep. 44:116028 (2025)

Verlagsversion

Forschungsdaten

DOI

PMC

	Open Access Gold

Abstract
Metriken
Zusatzinfos

Herein, we show a molecular pathway driven by an evolutionarily conserved microRNA (miRNA) in sensory neurons to control neuropathic pain. By employing high-throughput sequencing analysis, we find that miRNA-323-3p (miR-323-3p) exhibits the most significant upregulation in injured trigeminal ganglia (TGs). Local inhibition of miR-323-3p in injured TGs suppresses established trigeminal neuropathic pain but has no effect on inflammatory pain. Mechanistically, nerve injury upregulates the protein expression of protein arginine methyltransferase 2 (PRMT2), which promotes asymmetric dimethylation of H3R8, thereby facilitating the binding of the transcription factor forkhead box A2 (FOXA2) to the miR-323-3p promoter and resulting in the upregulation of miR-323-3p expression. Furthermore, the increased miR-323-3p expression induces significant reductions in Kv2.1 protein expression and channel currents, resulting in TG neuronal hyperexcitability. Conversely, the downregulation of miR-323-3p in injured TGs restores the decreased Kv2.1 expression and attenuates nerve-injury-induced mechanical hypersensitivity. The PRMT2/FOXA2/miR-323-3p/Kv2.1 signaling axis in sensory neurons may offer therapeutic targets in neuropathic pain management.

Impact Factor

Scopus SNIP

Altmetric

6.900

0.000