{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,19]],"date-time":"2026-08-19T18:59:20Z","timestamp":1787165960009,"version":"build-2736575974"},"reference-count":37,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2017,11,6]],"date-time":"2017-11-06T00:00:00Z","timestamp":1509926400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clin Exp Pharma Physio"],"published-print":{"date-parts":[[2018,1]]},"abstract":"Summary<\/jats:title>\n \n Spinal cord injury (\n SCI<\/jats:styled-content>\n ) is a major disability requiring more effective treatment than is currently available. Micro\n RNA<\/jats:styled-content>\n s 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\u201030\u20105p and possible mechanism in\n SCI<\/jats:styled-content>\n . We found that miR\u201030\u20105p was notably down\u2010regulated, while Neurod 1 expression was highly elevated in microglia from the mouse model of\n SCI<\/jats:styled-content>\n . Additionally, overexpression of miR\u201030a\u20105p significantly suppressed inflammatory responses as reflected by a decrease in the secretion of the cytokines\n TNF<\/jats:styled-content>\n \u2010\u03b1,\n IL<\/jats:styled-content>\n \u20101\u03b2 and\n IL<\/jats:styled-content>\n \u201010 triggered by\n SCI<\/jats:styled-content>\n . Furthermore, introduction of miR\u201030a\u20105p strengthened the scavenging of oxygen free radicals accompanied by an increase in the expression of\n SEPN<\/jats:styled-content>\n 1,\n TXNL<\/jats:styled-content>\n 1 and\n GPX<\/jats:styled-content>\n 1. More importantly, our study explored that Neurod 1 was a direct and functional target of miR\u201030a\u20105p, which was validated by the dual luciferase reporter assay.\n qRT<\/jats:styled-content>\n \u2010\n PCR<\/jats:styled-content>\n and western blot analysis further validated that miR\u201030a\u20105p negatively regulated the expression of Neurod 1. Mechanistically, overexpression of miR\u201030a\u20105p or silencing of the Neurod 1 gene prevented the\n MAPK<\/jats:styled-content>\n \/\n ERK<\/jats:styled-content>\n signalling and inhibited inflammatory responses, meanwhile activated\n SEPN<\/jats:styled-content>\n 1,\n TXNL<\/jats:styled-content>\n 1 and\n GPX<\/jats:styled-content>\n 1. These findings indicate that miR\u201030a\u20105p ameliorates inflammatory responses and oxidative stress by targeting Neurod 1 through\n MAPK<\/jats:styled-content>\n \/\n ERK<\/jats:styled-content>\n signalling.\n <\/jats:p>","DOI":"10.1111\/1440-1681.12856","type":"journal-article","created":{"date-parts":[[2017,9,19]],"date-time":"2017-09-19T06:33:07Z","timestamp":1505802787000},"page":"68-74","source":"Crossref","is-referenced-by-count":72,"title":["MiR\u201030a\u20105p ameliorates spinal cord injury\u2010induced inflammatory responses and oxidative stress by targeting Neurod 1 through\n MAPK<\/scp>\n \/\n ERK<\/scp>\n signalling"],"prefix":"10.1111","volume":"45","author":[{"given":"Xiaodong","family":"Fu","sequence":"first","affiliation":[{"name":"Department of Orthopedics School of Medicine South Campus, Renji Hospital Shanghai JiaoTong University Shanghai 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