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MiR‐30a‐5p ameliorates spinal cord injury‐induced inflammatory responses and oxidative stress by targeting Neurod 1 through MAPK/ERK signalling

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Spinal cord injury (SCI) is a major disability requiring more effective treatment than is currently available. MicroRNAs have been shown to effectively regulate gene expression at the translational level. The aim of the present study was to explore the potential role of miR‐30‐5p and possible mechanism in SCI. We found that miR‐30‐5p was notably down‐regulated, while Neurod 1 expression was highly elevated in microglia from the mouse model of SCI. Additionally, overexpression of miR‐30a‐5p significantly suppressed inflammatory responses as reflected by a decrease in the secretion of the cytokines TNF‐α, IL‐1β and IL‐10 triggered by SCI. Furthermore, introduction of miR‐30a‐5p strengthened the scavenging of oxygen free radicals accompanied by an increase in the expression of SEPN1, TXNL1 and GPX1. More importantly, our study explored that Neurod 1 was a direct and functional target of miR‐30a‐5p, which was validated by the dual luciferase reporter assay. qRT‐PCR and western blot analysis further validated that miR‐30a‐5p negatively regulated the expression of Neurod 1. Mechanistically, overexpression of miR‐30a‐5p or silencing of the Neurod 1 gene prevented the MAPK/ERK signalling and inhibited inflammatory responses, meanwhile activated SEPN1, TXNL1 and GPX1. These findings indicate that miR‐30a‐5p ameliorates inflammatory responses and oxidative stress by targeting Neurod 1 through MAPK/ERK signalling.
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Keywords: MAPK/ERK signalling; Neurod 1; inflammatory; miR‐30a‐5p; oxidative stress; spinal cord injury

Document Type: Research Article

Publication date: January 1, 2018

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