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miR-125a Suppresses TrxR1 Expression and Is Involved in H(2)O(2)-Induced Oxidative Stress in Endothelial Cells

Thioredoxin reductase (TrxR), an antioxidant enzyme dependent on nicotinamide adenine dinucleotide phosphate, plays a vital role in defense against oxidative stress. However, the role of microRNAs targeting TrxR under oxidative stress has not yet been determined. In this study, we tested the involve...

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Detalles Bibliográficos
Autores principales: Chen, Fangjie, Liu, Hong, Wu, Jingjing, Zhao, Yanyan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6129346/
https://www.ncbi.nlm.nih.gov/pubmed/30225271
http://dx.doi.org/10.1155/2018/6140320
Descripción
Sumario:Thioredoxin reductase (TrxR), an antioxidant enzyme dependent on nicotinamide adenine dinucleotide phosphate, plays a vital role in defense against oxidative stress. However, the role of microRNAs targeting TrxR under oxidative stress has not yet been determined. In this study, we tested the involvement of miRNA-mediated posttranscriptional regulation in H(2)O(2)-induced TrxR1 expression in endothelial cells. Dual luciferase assay combined with expression analysis confirmed that miR-125a suppressed TrxR1 expression by targeting its 3′-UTR. Furthermore, H(2)O(2) induced TrxR1 expression partly through downregulation of miR-125a. These findings indicate that miRNA-mediated posttranscriptional mechanism is involved in H(2)O(2)-induced TrxR1 expression in endothelial cells, suggesting an important role of miRNAs in the response to oxidative stress.