LINC00707 Silencing Alleviates Inflammation and Oxidative Stress in LPS-stimulated BV2 Microglia via the...

Spinal cord injury (SCI) causes lifelong disability, profoundly reduces well-being, and imposes a substantial socioeconomic burden. This study investigated the role of LINC00707 in SCI through regulation of the miR-145-5p/TRAF6 signaling axis. Plasma samples from 30 healthy subjects and 75 patients with SCI were analyzed for LINC00707, miR-145-5p, and TRAF6 expression using RT-qPCR. Associations between plasma LINC00707 levels and pro-inflammatory factors were assessed in patients with SCI. BV2 microglial cells were exposed to 100 ng/mL LPS, and inflammation- and oxidative stress-related factors were measured. Molecular interactions were assessed using a dual-luciferase reporter assay. Logistic regression analysis was used to identify factors associated with LINC00707 expression. Plasma LINC00707 and TRAF6 levels were increased in patients with SCI, whereas miR-145-5p levels were reduced. Plasma LINC00707 levels were positively correlated with plasma inflammatory factor levels. LINC00707 acted as a molecular sponge for miR-145-5p, and TRAF6 was a target gene of miR-145-5p. Inhibition of LINC00707 decreased inflammatory factors, pro-oxidative stress substances, and TRAF6 mRNA levels in BV2 cells. Inhibition of miR-145-5p produced the opposite effects. These findings suggest that elevated LINC00707 expression is associated with SCI severity and that LINC00707 knockdown may alleviate microglia-mediated inflammation and oxidative stress by regulating the miR-145-5p/TRAF6 signaling axis.