A5039770334- Nerve injury and regeneration
- Pain Mechanisms and Treatments
- Dermatology and Skin Diseases
- Cancer-related gene regulation
- RNA modifications and cancer
- IL-33, ST2, and ILC Pathways
- Neuropeptides and Animal Physiology
- Signaling Pathways in Disease
- Hereditary Neurological Disorders
Soochow University
2022-2024
Second Affiliated Hospital of Soochow University
2022
The N6-methyladenosine (m 6 A) modification of RNA is an emerging epigenetic regulatory mechanism that has been shown to participate in various pathophysiological processes. However, its involvement modulating neuropathic pain still poorly understood. In this study, we elucidate a functional role the m A demethylase alkylation repair homolog 5 (ALKBH5) trigeminal-mediated pain. Peripheral nerve injury selectively upregulated expression level ALKBH5 injured trigeminal ganglion (TG) rats....
Significance In this study, we identify microRNA-32-5p (miR-32-5p) as a key functional noncoding RNA in trigeminal-mediated neuropathic pain. We report that injury-induced histone methylation attenuates the binding of glucocorticoid receptor to promoter region miR-32-5p gene and decreases expression miR-32-5p, turn promoting development pain through regulation Cav3.2 channels. miRNA-mediated has been proposed therapeutic approach Our findings replenishment strategy for treating chronic
Abstract Although beta-endorphinergic neurons in the hypothalamic arcuate nucleus (ARC) synthesize beta-endorphin (β-EP) to alleviate nociceptive behaviors, underlying regulatory mechanisms remain unknown. Here, we elucidated an epigenetic pathway driven by microRNA regulation of β-EP synthesis ARC control neuropathic pain. In pain-injured rats miR-203a-3p was most highly upregulated miRNA ARC. A similar increase identified cerebrospinal fluid trigeminal neuralgia patients. Mechanistically,...
Background: has been implicated in nociceptive pain behaviors.However, the underlying molecular and cellular mechanisms remain unclear.Methods: Using electrophysiological recording, immunoblot analysis, immunofluorescence labeling, reverse transcription-PCR, siRNA-mediated knockdown approach behavior tests, we determined role of IL-33 regulating sensory neuronal excitability sensitivity mediated by A-type K + channels.Results: decreased transient outward currents (IA) small-sized DRG neurons...