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Copyright (c) 2023 Weihong Mao, Xiaoming Wang, Yongchen Zhang, Huding Zhu, Li Dai, Juanjuan Chen
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
The undersigned hereby assign all rights, included but not limited to copyright, for this manuscript to CMB Association upon its submission for consideration to publication on Cellular and Molecular Biology. The rights assigned include, but are not limited to, the sole and exclusive rights to license, sell, subsequently assign, derive, distribute, display and reproduce this manuscript, in whole or in part, in any format, electronic or otherwise, including those in existence at the time this agreement was signed. The authors hereby warrant that they have not granted or assigned, and shall not grant or assign, the aforementioned rights to any other person, firm, organization, or other entity. All rights are automatically restored to authors if this manuscript is not accepted for publication.Nuclear factor-kappa B p50-induced microRNA-20a-3p plays a detrimental role in sepsis-induced acute kidney injury
Corresponding Author(s) : Huding Zhu
Cellular and Molecular Biology,
Vol. 69 No. 8: Issue 8
Abstract
Sepsis is the most common cause of acute kidney injury (AKI). Based on microarray-based clustering analysis of miRNAs altered in the kidneys of LPS-AKI mice, miR-20a-3p was upregulated in the kidney tissues of lipopolysaccharide (LPS)-treated mice. We aimed to reveal the functions of miR-20a-3p in septic AKI by establishing the LPS-stimulated mouse model of AKI and constructing the LPS-stimulated HK-2 cells. Reverse transcription-quantitative PCR was used to quantify miR-20a-3p expression and inflammation-associated factors including MCP-1, TNF-α, and IL-6. Silencing of miR-20a-3p reduced inflammation and apoptosis in kidneys as well as alleviated AKI symptoms in mice. The LPS-induced inflammatory response and apoptosis in HK-2 cells were rescued by miR-20a-3p silence. Moreover, nuclear factor-kappa B (NF-κB) is a transcriptional factor for miR-20a-3p to increase its expression. The binding of NF-κB p50 and miR-20a-3p promoter was verified by ChIP assay. To sum up, miR-20a-3p is transcriptionally activated by NF-κB p50, playing a harmful role in sepsis-induced AKI by inducing inflammation and apoptosis.
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