ArticleApplied biochemistry and biotechnology2026
LncRNA UCA1 Aggravated Microglia-mediated Neuroinflammation After Traumatic Brain Injury by Targeting miR-708-5p.
Article in Applied biochemistry and biotechnology, 2026. 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
Secondary neuroinflammation following traumatic brain injury (TBI) is the key factor leading to neurological deterioration. LncRNA UCA1 exerts regulatory effects in multiple pathological processes, but its specific function and mechanism in TBI remain unclear. The aim of this study was to explore the role of UCA1 in neuroinflammation following TBI and to verify whether it regulates neural injury by miR-708-5p. The inflammatory model was built in BV-2 microglia by LPS stimulation. Transfection was utilized to regulate UCA1 and miR-708-5p expression in cells. CCK-8, flow cytometry, ELISA, and dual luciferase reporter assay were employed to evaluate cell viability, apoptosis, inflammatory factors, and targeting relationship. A mouse TBI model was established via controlled cortical impact. The expression of UCA1 and miR-708-5p in mice was interfered by injecting sh-UCA1 lentivirus and miR-708-5p antagomir. The neurological severity score, Morris water maze test, brain-water content, and inflammatory factors levels in brain tissue were assessed in mice from different treatment groups. UCA1 expression was upregulated in TBI patient serum. Cell experiments indicated that silencing UCA1 markedly inhibited LPS-induced apoptosis and inflammatory cytokine release in BV-2 cells. In vivo experiments showed that silencing UCA1 improved neurological deficits, spatial memory impairment, cerebral edema, and inflammatory responses in TBI mice. Dual luciferase reporter assays revealed that UCA1 directly targets and binds to miR-708-5p, and that miR-708-5p directly targets TLR4. Mechanistically, inhibition of miR-708-5p partially reversed the protective effect induced by silencing UCA1, and this effect was mediated at least in part through TLR4. UCA1 promotes microglial-mediated neuroinflammation and injury after TBI by negatively regulating miR-708-5p and subsequently modulating TLR4. Targeting the UCA1/miR-708-5p/TLR4 axis may offer new therapeutic strategies for TBI.
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