ArticleApplied biochemistry and biotechnology2025
lncRNA SNHG6 Knockdown Promotes Microglial M2 Polarization and Alleviates Spinal Cord Injury via Regulating the miR-182-5p/NEUROD4 Axis.
Article in Applied biochemistry and biotechnology, 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
Spinal cord injury (SCI) is one of the devastating neurological disorders that leads to a loss of motor and sensory functions. Long non-coding RNA small nucleolar RNA host gene 6 (lncRNA SNHG6) plays a crucial role in inflammatory regulation across various diseases. This study investigates the role of SNHG6 in SCI development and its underlying regulatory mechanisms. Two experimental models were established: an in vitro model using LPS-challenged (100 ng/mL) mouse microglia BV2 cells and an in vivo model employing controlled spinal cord impact in mice. SNHG6, miR-182-5p, and NEUROD4 expression levels were quantified through RT-qPCR and Western blot. Functional and histological assessments were performed using the Basso mouse scale (BMS) and Nissl staining, respectively. Putative binding sites between SNHG6 and miR-182-5p, as well as between miR-182-5p and NEUROD4, were predicted using the ENCORI/starBase platform. These molecular interactions were validated through dual-luciferase reporter assays and RNA pull-down experiments, with further confirmation by qRT-PCR and Western blot analyses. Both LPS-stimulated BV2 cells and spinal cord tissues from SCI mice exhibited elevated SNHG6 expression. Downregulation of SNHG6 enhanced LPS-induced polarization of BV2 cells from M1-type to M2-type, significantly modulated the expression of pro-inflammatory factors (TNF-α, IL-1β, and IL-6) and anti-inflammatory factors (TGF-β, IL-10, and IL-13), and reduced injury severity in SCI mice. Our mechanistic studies revealed that SNHG6 functions as a molecular sponge for miR-182-5p to regulate NEUROD4 expression. This study demonstrates that SNHG6 knockdown promotes microglial M2-type polarization and alleviates inflammatory responses through modulation of the miR-182-5p/NEUROD4 axis, suggesting SNHG6 as a potential therapeutic target for SCI treatment.
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