OBJECTIVE The aim of this study was to investigate the mechanisms of TUSC7/miR-449a/PPAR-γ axis on the inflammation induced by microglia activation. METHODS A compressive spinal cord injury (SCI) model was… Click to show full abstract
OBJECTIVE The aim of this study was to investigate the mechanisms of TUSC7/miR-449a/PPAR-γ axis on the inflammation induced by microglia activation. METHODS A compressive spinal cord injury (SCI) model was established. The expressions of TUSC7, miR-449a PPAR-γ, TNF-α and IL-1β in spinal cord tissues of SCI rats and HAPI cells were determined. The interaction of TUSC7 and miR-449a was tested by RIP and RNA pull-down assays. The regulatory relationship between miR-449a and PPAR-γ was tested by dual luciferase reporter gene assay. RESULTS In the spinal cord tissue of SCI rats and HAPI cells induced by LPS, TUSC7 expression was reduced and miR-449a expression was increased. Overexpression of TUSC7 inhibited microglial activation and the expression of inflammatory factors (TNF-α and IL-1β). Moreover, we have found a targeting regulatory relation between TUSC7 and miR-449a, and a negative regulatory relationship between miR-449a and PPAR-γ. In the study of molecular mechanism, we found that TUSC7 could regulate PPAR-γ through miR-449a, and overexpression of TUSC7 inhibited microglial activation and the expression of inflammatory factors through miR-449a. CONCLUSION Overexpression of TUSC7 inhibited microglial activation and the expression of inflammatory factors in microglia cells by regulating miR-449a/PPAR-γ.
               
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