LncRNA MIR155HG suppresses cell apoptosis by activating autophagy via miR-7036b-3p/GPNMB axis and AMPK/mTOR signaling in spinal cord injury.

BACKGROUND

Long non-coding RNAs (lncRNAs) participate in spinal cord injury (SCI) development through regulating autophagy and neuronal apoptosis. Previously, was identified as an upregulated lncRNA in rat bladder tissues harvested after SCI operation. Our study aimed to elucidate the function of in SCI.

METHODS

Glutamate (Glu)-stimulated primary mouse spinal cord neurons were used as SCI cellular models. Contusion-induced SCI mouse models were established using an improved weightlessness method. Neuronal apoptosis and autophagy affected by or silencing were assessed by TUNEL staining, flow cytometry assay, western blotting, and immunofluorescence staining. The binding of miR-7036b-3p on (or ) was verified by luciferase reporter assay. Histological changes were observed through HE and Masson staining.

RESULTS

and expression was elevated while miR-7036b-3p expression was reduced in SCI. silencing attenuated the apoptosis in Glu-stimulated neurons and ameliorated glial scar formation and motor function of SCI mice. knockdown mitigated apoptosis, enhanced autophagy, activated AMPK phosphorylation, and repressed mTOR phosphorylation. upregulated expression by sponging miR-7036b-3p. The autophagy inhibitor 3-MA reversed the above changes caused by depletion.

CONCLUSION

knockdown alleviated neuronal apoptosis by enhancing autophagy in SCI via miR-7036b-3p/ axis and AMPK/mTOR pathway.