Knockdown of lncRNA TapSAKI alleviates LPS-induced injury in HK-2 cells through the miR-205/IRF3 pathway

Sepsis is a common and lethal syndrome. Long non-coding RNA (lncRNA) transcript predicting survival in AKI (TapSAKI) has recently been found to serve as an important regulator in sepsis. However, the underlying mechanism of TapSAKI in sepsis pathogenesis remains largely unknown. Our data demonstrate...

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Autores principales: Han Xiaoning, Yuan Zhiyong, Jing Yajun, Zhou Weigui, Sun Yunbo, Xing Jinyan
Formato: article
Lenguaje:EN
Publicado: De Gruyter 2021
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Acceso en línea:https://doaj.org/article/a80d9cb1a5044e299f6401115dc30a30
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spelling oai:doaj.org-article:a80d9cb1a5044e299f6401115dc30a302021-12-05T14:10:53ZKnockdown of lncRNA TapSAKI alleviates LPS-induced injury in HK-2 cells through the miR-205/IRF3 pathway2391-546310.1515/med-2021-0204https://doaj.org/article/a80d9cb1a5044e299f6401115dc30a302021-04-01T00:00:00Zhttps://doi.org/10.1515/med-2021-0204https://doaj.org/toc/2391-5463Sepsis is a common and lethal syndrome. Long non-coding RNA (lncRNA) transcript predicting survival in AKI (TapSAKI) has recently been found to serve as an important regulator in sepsis. However, the underlying mechanism of TapSAKI in sepsis pathogenesis remains largely unknown. Our data demonstrated that lipopolysaccharide (LPS)-induced HK-2 cell injury by weakening cell viability and enhancing cell apoptosis and inflammation. TapSAKI was upregulated and miR-205 was downregulated in LPS-induced HK-2 cells. TapSAKI knockdown or miR-205 overexpression alleviated LPS-induced cytotoxicity in HK-2 cells. TapSAKI sequestered miR-205 via acting as a miR-205 sponge. Moreover, the mitigating effect of TapSAKI silencing on LPS-induced HK-2 cell injury was mediated by miR-205. Additionally, the interferon regulatory factor 3 (IRF3) signaling was involved in the regulation of the TapSAKI/miR-205 axis on LPS-induced HK-2 cell damage. Our current study suggested that TapSAKI silencing relieved LPS-induced injury in HK-2 cells at least in part by sponging miR-205 and regulating the IRF3 signaling pathway, highlighting a novel understanding for sepsis pathogenesis and a promising target for this disease treatment.Han XiaoningYuan ZhiyongJing YajunZhou WeiguiSun YunboXing JinyanDe Gruyterarticlesepsistapsakimir-205lpscell injuryMedicineRENOpen Medicine, Vol 16, Iss 1, Pp 581-590 (2021)
institution DOAJ
collection DOAJ
language EN
topic sepsis
tapsaki
mir-205
lps
cell injury
Medicine
R
spellingShingle sepsis
tapsaki
mir-205
lps
cell injury
Medicine
R
Han Xiaoning
Yuan Zhiyong
Jing Yajun
Zhou Weigui
Sun Yunbo
Xing Jinyan
Knockdown of lncRNA TapSAKI alleviates LPS-induced injury in HK-2 cells through the miR-205/IRF3 pathway
description Sepsis is a common and lethal syndrome. Long non-coding RNA (lncRNA) transcript predicting survival in AKI (TapSAKI) has recently been found to serve as an important regulator in sepsis. However, the underlying mechanism of TapSAKI in sepsis pathogenesis remains largely unknown. Our data demonstrated that lipopolysaccharide (LPS)-induced HK-2 cell injury by weakening cell viability and enhancing cell apoptosis and inflammation. TapSAKI was upregulated and miR-205 was downregulated in LPS-induced HK-2 cells. TapSAKI knockdown or miR-205 overexpression alleviated LPS-induced cytotoxicity in HK-2 cells. TapSAKI sequestered miR-205 via acting as a miR-205 sponge. Moreover, the mitigating effect of TapSAKI silencing on LPS-induced HK-2 cell injury was mediated by miR-205. Additionally, the interferon regulatory factor 3 (IRF3) signaling was involved in the regulation of the TapSAKI/miR-205 axis on LPS-induced HK-2 cell damage. Our current study suggested that TapSAKI silencing relieved LPS-induced injury in HK-2 cells at least in part by sponging miR-205 and regulating the IRF3 signaling pathway, highlighting a novel understanding for sepsis pathogenesis and a promising target for this disease treatment.
format article
author Han Xiaoning
Yuan Zhiyong
Jing Yajun
Zhou Weigui
Sun Yunbo
Xing Jinyan
author_facet Han Xiaoning
Yuan Zhiyong
Jing Yajun
Zhou Weigui
Sun Yunbo
Xing Jinyan
author_sort Han Xiaoning
title Knockdown of lncRNA TapSAKI alleviates LPS-induced injury in HK-2 cells through the miR-205/IRF3 pathway
title_short Knockdown of lncRNA TapSAKI alleviates LPS-induced injury in HK-2 cells through the miR-205/IRF3 pathway
title_full Knockdown of lncRNA TapSAKI alleviates LPS-induced injury in HK-2 cells through the miR-205/IRF3 pathway
title_fullStr Knockdown of lncRNA TapSAKI alleviates LPS-induced injury in HK-2 cells through the miR-205/IRF3 pathway
title_full_unstemmed Knockdown of lncRNA TapSAKI alleviates LPS-induced injury in HK-2 cells through the miR-205/IRF3 pathway
title_sort knockdown of lncrna tapsaki alleviates lps-induced injury in hk-2 cells through the mir-205/irf3 pathway
publisher De Gruyter
publishDate 2021
url https://doaj.org/article/a80d9cb1a5044e299f6401115dc30a30
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AT yuanzhiyong knockdownoflncrnatapsakialleviateslpsinducedinjuryinhk2cellsthroughthemir205irf3pathway
AT jingyajun knockdownoflncrnatapsakialleviateslpsinducedinjuryinhk2cellsthroughthemir205irf3pathway
AT zhouweigui knockdownoflncrnatapsakialleviateslpsinducedinjuryinhk2cellsthroughthemir205irf3pathway
AT sunyunbo knockdownoflncrnatapsakialleviateslpsinducedinjuryinhk2cellsthroughthemir205irf3pathway
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