MiR-181a-5p Alleviates the Inflammatory Response of PC12 Cells by Inhibiting High-Mobility Group Box-1 Protein Expression

Abstract

Neuroinflammation triggers sequelae after spinal cord injury (SCI). Inhibition of inflammation promotes recovery after SCI. MicroRNAs regulate many pathophysiological processes, including inflammation. Any role for miR-181a-5p in the inflammatory response after SCI remains unclear. Thus, we evaluated the effects of miR-181a-5p on inflammation in PC12cells and the underlying mechanism in play. Quantitative reverse transcription-polymerase chain reaction was used to measure the levels of miR-181a-5p and high-mobility group box-1 protein (HMGB1) in SCI tissues. Cell-counting kit-8 assays were used to assess the viability of PC12cells treated with lipopolysaccharide (LPS). Plasmids encoding MiR-181a-5p mimics, an miR-181a-5p inhibitor, or/and the HMGB1 weretransfected into PC12cells. Quantitative reverse transcription-polymerase chain reaction or/and Western blotting were performed to assess the expression of miR-181a-5p, HMGB1, and inflammatory factors invitro. MiR-181a-5p expression decreased and HMGB1 expression increased in SCI tissues and LPS-induced PC12cells. Upregulation of miR-181a-5p (via transfection) inhibited inflammation of, and HMGB1 expression by, LPS-induced PC12cells. HMGB1 overexpression reversed the anti-inflammatory effects of miR-181a-5p. Dual-luciferase assays confirmed that HMGB1 was a direct target of miR-181a-5p. miR-181a-5p attenuated the inflammatory response of LPS-induced PC12cells by directly inhibiting HMGB1; thus, miR-181a-5p may serve as a therapeutic target in SCI.