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• W2920285540 startingPage "11582" @default.
• W2920285540 abstract "Spinal cord injury (SCI) has been a major burden on the society because of the high rate of disability. Receptor-interacting protein 3 (RIP3)-mediated necroptosis is a newly discovered pathway of programmed cell death and is involved in multiple pathologies of various human diseases. Micro RNAs (miRNAs) have been shown to be a potential target for therapeutic interventions after SCI. The aim of the present study is to explore the potential role of miR-223-3p and possible mechanism in SCI. We found that miR-223-3p was significantly downregulated in spinal neurons after H2 O 2 -induced damage, while RIP3-mediated necroptosis was elevated. Accordingly, RIP3-mediated necroptosis and the inflammatory factor secretion could be significantly inhibited by Nec-1 treatment. In adittion, overexpression of miR-223-3p in spinal neurons protected against H 2 O 2 -induced necroptosis, and ablation of miR-223-3p exhibited the opposite effect. We found that miR-223-3p bound to the 3'-untranslated region of RIP3 mRNA to negatively regulate the expression of RIP3. Moreover, the activated RIP3 reversed the inhibition of RIP3 and MLKL expression and the levels of TNF-α, IL-1β, and lactate dehydrogenase, which were induced by transfection with miR-223-3p in a H 2 O 2 -induced model. Finally, these results indicate that miR-223-3p negatively regulates the RIP3 necroptotic signaling cascades and inflammatory factor secretion, which significantly relieves injury of spinal neurons. The miR-223-3p/RIP3 pathway offers a novel therapeutic target for the protection of spinal neurons after SCI." @default.
• W2920285540 created "2019-03-11" @default.
• W2920285540 creator A5008889856 @default.
• W2920285540 creator A5017301514 @default.
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• W2920285540 date "2019-02-28" @default.
• W2920285540 modified "2023-10-16" @default.
• W2920285540 title "Upregulation of miRNA‐223‐3p ameliorates RIP3‐mediated necroptosis and inflammatory responses via targeting RIP3 after spinal cord injury" @default.
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• W2920285540 doi "https://doi.org/10.1002/jcb.28438" @default.
• W2920285540 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30821011" @default.
• W2920285540 hasPublicationYear "2019" @default.
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