Abstract
Background: Spinal cord injury (SCI) can cause severe motor and sensory deficits below the injury site. Studies have highlighted the multifaceted regulatory roles of miR-29c-3p in neuronal development and function; however, its role in SCI remains unclear. Methods: In this research 105 healthy controls and 159 patients with SCI were recruited. The miR-29c-3p and BRD4 levels in serum or cells were estimated by RT-qPCR. The diagnostic performance of miR-29c-3p was assessed by ROC curve. Moreover, cell viability and apoptosis were measured via CCK8 and flow cytometry. The pro-inflammatory cytokines were examined by ELISA assay. The pathological condition of SCI was modeled with LPS-induced PC12 cells. The target relationship between miR-29c-3p and BRD4 was verified by the dual-luciferase reporter assay. Results: Serum miR-29c-3p was remarkedly decreased in the SCI population and showed high clinical diagnostic performance. Under pathological conditions, the upregulation of miR-29c-3p effectively reversed the significant reduction in cell viability and the increase in apoptosis rate. Moreover, enhanced pro-inflammatory cytokines including TNF-α, IL-6 and IL-1β were also attenuated by the upregulation of miR-29c-3p. BRD4 was identified as a target of miR-29c-3p and negatively regulated by miR-29c-3p. Conclusions: A decrease in miR-29c-3p is a promising diagnostic indicator for SCI, and downregulation of miR-29c-3p accelerates the progression of SCI by targeting BRD4.