ArticleBioscience reports2021
GCH1-regulated miRNAs are potential targets for microglial activation in neuropathic pain.
Article in Bioscience reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- A Systematic Bioinformatic Analysis of the miRNA Pathway in Inborn Errors of Amino Acid Metabolism Disorders.Molecular syndromology · 2026Article
- Microglia-derived neuroinflammatory pathways in neuropathic pain.The Korean journal of pain · 2026Review
- A Comprehensive microRNA-seq Transcriptomic Analysis of Tay-Sachs Disease Mice Revealed Distinct miRNA Profiles in Neuroglial Cells.Journal of molecular neuroscience : MN · 2025Article
- Screening for biomarkers of bronchopulmonary dysplasia: a bioinformatics analysis.Translational pediatrics · 2025Article
- Exosome-mediated miRNA delivery: a molecular switch for reshaping neuropathic pain therapy.Frontiers in molecular neuroscience · 2025Review
- New Insight into Neuropathic Pain: The Relationship between α7nAChR, Ferroptosis, and Neuroinflammation.International journal of molecular sciences · 2024Review
- Intrathecal liproxstatin-1 delivery inhibits ferroptosis and attenuates mechanical and thermal hypersensitivities in rats with complete Freund's adjuvant-induced inflammatory pain.Neural regeneration research · 2023Article
- UPLC-Q-TOF/MS Based Plasma Metabolomics for Identification of Paeonol's Metabolic Target in Endometriosis.Molecules (Basel, Switzerland) · 2023Article
- GCH1 Deficiency Activates Brain Innate Immune Response and Impairs Tyrosine Hydroxylase Homeostasis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Sirtuin 2 Alleviates Chronic Neuropathic Pain by Suppressing Ferroptosis in Rats.Frontiers in pharmacology · 2022Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
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Abstract
Neuropathic pain (NP) is a chronic pain directly caused by injury or disease of the somatosensory nervous system. Previous studies suggest that GTP cyclohydrolase I (GCH1) may play a pivotal role in microglial activation, which has been shown to be essential for NP. However, its underlying mechanisms in microglial activation remain unclear. A wide range of microRNAs (miRNAs) have been found to be involved in microglial activation-induced NP. To identify the miRNAs regulated by GCH1 and predict their functions in the progression of microglial activation, we analyzed the miRNA expression profiles of GCH1-knockdown (KD) BV2 microglial cells. Small RNA-sequencing analysis revealed 13 differentially expressed (DE) miRNAs in GCH1-KD cells. The target genes of DE miRNAs mainly participate in PI3K-Akt signaling pathway, peroxisome and ferroptosis. The miRNA-mRNA regulatory network analysis showed that GCH1, MAP4K5 and YWHAB acted as hub genes. qRT-PCR results further verified the expression levels of mmu-miR-1a-3p, mmu-miR-133a-3p, mmu-miR-7a-5p and mmu-miR-10a-5p in GCH1-KD cells, which were consistent with the sequencing data. In addition, our data indicated that overexpression of mmu-miR-133a-3p alleviated the pro-inflammatory cytokines IL-1β and IL-6 production induced by lipopolysaccharide (LPS), indicating that mmu-miR-133a-3p has a negative effect on microglial activation. Taken together, our findings suggest that many miRNAs regulated by GCH1 may be involved in microglial activation, which may provide new potential targets for GCH1 in the pathogenesis of NP.
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