ArticleMolecular neurobiology2025
Exploring the Role of Microglia Activation in Ischemia Stroke Based on the circDnajc1/miR-27a-5p/C1qc Signaling Axis.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
To date, our understanding of the relationship between middle cerebral artery occlusion/reperfusion (MCAO/R)-induced ischemia stroke and circular RNAs (circRNAs) remains limited. The objective of this research was to explore the roles and underlying mechanisms of the circDnajc1/miR-27a-5p/C1qc signaling pathway in the development of ischemia stroke. For in vitro experiments, an oxygen-glucose deprivation/reperfusion (OGD/R) cell model was established following neuron-microglia co-culture. circDnajc1 siRNA and pcDNA3.1-circDnajc1 overexpression vectors were constructed and transfected into primary microglia. For in vivo experiments, an MCAO/R rat model was established. The molecular mechanisms were investigated using flow cytometry, RT-qPCR, immunofluorescence, RNA immunoprecipitation, and luciferase reporter gene assays. In vitro experiments showed that circDnajc1-induced cellular activation following microglia OGD/R injury, promoted the release of inflammatory factors, downregulated miR-27a-5p, upregulated C1qc, C3, and C5ar, and promotes neuronal apoptosis after microglia OGD/R injury. Interference with circDnajc1 reversed these effects. In vivo experiments, circDnajc1 knockdown exerted a protective effect on neurons in MCAO/R rats and inhibited microglial activation and the release of inflammatory factors. Consistent with the in vitro experiments, circDnajc1 regulated on the expression of downstream target genes of miR-27a-5p, C1qc, C3, and C5ar. CircDnajc1 plays a critical role in ischemia stroke and may influence nervous system homeostasis by regulating the circDnajc1/miR-27a-5p/C1qc signaling axis, which promotes microglia activation and regulates inflammatory factor release and neuronal apoptosis.
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