Silencing miR-134-5p promotes functional recovery after spinal cord injury by activating brain-derived neurotrophic...

This study aimed to investigate the roles of miR-134-5p and BDNF in neuroinflammation, apoptosis, and motor function recovery after spinal cord injury (SCI).

A rat SCI model was established, and motor function recovery was evaluated using Basso-Beattie-Bresnahan (BBB) and inclined plane test (IPT) scores. An in vitro model was established using lipopolysaccharide (LPS)-stimulated PC12 cells. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to measure the expression levels of miR-134-5p and BDNF. Cell Counting Kit-8 (CCK-8) assays and flow cytometry were used to determine cell viability and apoptosis. Enzyme-linked immunosorbent assays (ELISAs) and RT-qPCR were used to quantify levels of inflammatory factors and apoptosis-related genes. Bioinformatics analysis identified BDNF as a target gene of miR-134-5p, and this interaction was further verified using dual-luciferase reporter (DLR) and RNA immunoprecipitation (RIP) assays.

LPS exposure elevated miR-134-5p expression and inhibited BDNF expression in PC12 cells. In rats with SCI, miR-134-5p was upregulated while BDNF was downregulated. Knockdown of miR-134-5p significantly promoted cell viability, decreased apoptosis, and alleviated inflammatory cytokine release. Mechanistically, miR-134-5p directly targeted and inhibited BDNF, and BDNF knockdown abolished the protective effects induced by miR-134-5p silencing. In vivo, downregulation of BDNF offset the anti-inflammatory and locomotor recovery effects mediated by miR-134-5p inhibition in SCI rats.

miR-134-5p aggravates neuroinflammation and apoptosis after SCI by targeting BDNF, and silencing miR-134-5p shows therapeutic potential through BDNF-mediated neuroprotection to alleviate injury and promote repair.