Journal of orthopaedic surgery and research · 2026
circ_0044235 exacerbates neuroinflammation and apoptosis following spinal cord injury by targeting miR-338-5p.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Lin Mianlong, Huang Lina, Zhang Bin, Wang Yue, Zhu Xingyu, Zeng Wencong
Аннотация
BACKGROUND: Spinal cord injury (SCI) triggers a cascade of secondary damages, including neuroinflammation and apoptosis, which critically impede neurological recovery. This study aims to investigate the function of circ_0044235 in this pathological process.
METHODS: In this study, an in vitro injury model was established by stimulating PC-12 cells with lipopolysaccharide (LPS), and an in vivo SCI model was prepared by the rat T9-10 percussion method. The recovery of motor function in rats was evaluated by BBB score. RT-qPCR was used to determine the levels of circ_0044235, miR-338-5p, and mRNA. Cell viability and apoptosis were detected by MTT and flow cytometry. ELISA was used to determine the levels of inflammatory factors. The interaction between circ_0044235 and miR-338-5p was verified by dual-luciferase reporter gene and RNA pull-down.
RESULT: LPS treatment up-regulated circ_0044235 expression and exacerbated PC-12 cell injury in a concentration-dependent manner. Silencing circ_0044235 improved cell viability, suppressed apoptosis, and reduced inflammatory factor release. Mechanistically, circ_0044235 directly bound to and negatively regulated miR-338-5p, with rescue experiments confirming its pro-injury role via miR-338-5p sponging. In vivo, knockdown of circ_0044235 promoted motor function recovery and reduced inflammation; these effects were reversed by a miR-338-5p antagomir. LRP1 was further identified as a direct downstream target of miR-338-5p.
CONCLUSION: circ_0044235 functions as a key pro-injury factor in SCI. It directly targets and adsorbs miR-338-5p, thereby exacerbating the neuroinflammatory response and the process of apoptosis, and ultimately hindering the recovery of neural function.
METHODS: In this study, an in vitro injury model was established by stimulating PC-12 cells with lipopolysaccharide (LPS), and an in vivo SCI model was prepared by the rat T9-10 percussion method. The recovery of motor function in rats was evaluated by BBB score. RT-qPCR was used to determine the levels of circ_0044235, miR-338-5p, and mRNA. Cell viability and apoptosis were detected by MTT and flow cytometry. ELISA was used to determine the levels of inflammatory factors. The interaction between circ_0044235 and miR-338-5p was verified by dual-luciferase reporter gene and RNA pull-down.
RESULT: LPS treatment up-regulated circ_0044235 expression and exacerbated PC-12 cell injury in a concentration-dependent manner. Silencing circ_0044235 improved cell viability, suppressed apoptosis, and reduced inflammatory factor release. Mechanistically, circ_0044235 directly bound to and negatively regulated miR-338-5p, with rescue experiments confirming its pro-injury role via miR-338-5p sponging. In vivo, knockdown of circ_0044235 promoted motor function recovery and reduced inflammation; these effects were reversed by a miR-338-5p antagomir. LRP1 was further identified as a direct downstream target of miR-338-5p.
CONCLUSION: circ_0044235 functions as a key pro-injury factor in SCI. It directly targets and adsorbs miR-338-5p, thereby exacerbating the neuroinflammatory response and the process of apoptosis, and ultimately hindering the recovery of neural function.