PLK1 protects against sepsis-induced intestinal barrier dysfunction

Abstract Sepsis and sepsis-associated intestinal barrier dysfunction are common in intensive care units, with high mortality. The aim of this study is to investigate whether Polo-like kinase 1 (PLK1) ameliorates sepsis-induced intestinal barrier dysfunction in the intestinal epithelium. The mouse in...

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Autores principales: Yingya Cao, Qun Chen, Zhen Wang, Tao Yu, Jingyi Wu, Xiaogan Jiang, Xiaoju Jin, Weihua Lu
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Publicado: Nature Portfolio 2018
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Acceso en línea:https://doaj.org/article/7e63f768a0bb4f0a9fb1b82146717c3a
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spelling oai:doaj.org-article:7e63f768a0bb4f0a9fb1b82146717c3a2021-12-02T15:07:46ZPLK1 protects against sepsis-induced intestinal barrier dysfunction10.1038/s41598-018-19573-x2045-2322https://doaj.org/article/7e63f768a0bb4f0a9fb1b82146717c3a2018-01-01T00:00:00Zhttps://doi.org/10.1038/s41598-018-19573-xhttps://doaj.org/toc/2045-2322Abstract Sepsis and sepsis-associated intestinal barrier dysfunction are common in intensive care units, with high mortality. The aim of this study is to investigate whether Polo-like kinase 1 (PLK1) ameliorates sepsis-induced intestinal barrier dysfunction in the intestinal epithelium. The mouse intestinal barrier was disrupted after Lipopolysaccharide (LPS) injection due to intestinal epithelial cell apoptosis and proliferation inhibition, accompanied by decreased PLK1. In HT-29 intestinal epithelial cells, LPS stimulation induced cell apoptosis and inhibited cell proliferation. Overexpression of PLK1 partly rescued the apoptosis and proliferation inhibition in HT29 cells caused by LPS. Finally, LPS stimulation promoted the reduction of PLK1, resulting in apoptosis and proliferation inhibition in intestinal epithelial cells, disrupting the intestinal epithelial barrier. These findings indicate that PLK1 might be a potential therapeutic target for the treatment of sepsis-induced intestinal barrier dysfunction.Yingya CaoQun ChenZhen WangTao YuJingyi WuXiaogan JiangXiaoju JinWeihua LuNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 8, Iss 1, Pp 1-8 (2018)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Yingya Cao
Qun Chen
Zhen Wang
Tao Yu
Jingyi Wu
Xiaogan Jiang
Xiaoju Jin
Weihua Lu
PLK1 protects against sepsis-induced intestinal barrier dysfunction
description Abstract Sepsis and sepsis-associated intestinal barrier dysfunction are common in intensive care units, with high mortality. The aim of this study is to investigate whether Polo-like kinase 1 (PLK1) ameliorates sepsis-induced intestinal barrier dysfunction in the intestinal epithelium. The mouse intestinal barrier was disrupted after Lipopolysaccharide (LPS) injection due to intestinal epithelial cell apoptosis and proliferation inhibition, accompanied by decreased PLK1. In HT-29 intestinal epithelial cells, LPS stimulation induced cell apoptosis and inhibited cell proliferation. Overexpression of PLK1 partly rescued the apoptosis and proliferation inhibition in HT29 cells caused by LPS. Finally, LPS stimulation promoted the reduction of PLK1, resulting in apoptosis and proliferation inhibition in intestinal epithelial cells, disrupting the intestinal epithelial barrier. These findings indicate that PLK1 might be a potential therapeutic target for the treatment of sepsis-induced intestinal barrier dysfunction.
format article
author Yingya Cao
Qun Chen
Zhen Wang
Tao Yu
Jingyi Wu
Xiaogan Jiang
Xiaoju Jin
Weihua Lu
author_facet Yingya Cao
Qun Chen
Zhen Wang
Tao Yu
Jingyi Wu
Xiaogan Jiang
Xiaoju Jin
Weihua Lu
author_sort Yingya Cao
title PLK1 protects against sepsis-induced intestinal barrier dysfunction
title_short PLK1 protects against sepsis-induced intestinal barrier dysfunction
title_full PLK1 protects against sepsis-induced intestinal barrier dysfunction
title_fullStr PLK1 protects against sepsis-induced intestinal barrier dysfunction
title_full_unstemmed PLK1 protects against sepsis-induced intestinal barrier dysfunction
title_sort plk1 protects against sepsis-induced intestinal barrier dysfunction
publisher Nature Portfolio
publishDate 2018
url https://doaj.org/article/7e63f768a0bb4f0a9fb1b82146717c3a
work_keys_str_mv AT yingyacao plk1protectsagainstsepsisinducedintestinalbarrierdysfunction
AT qunchen plk1protectsagainstsepsisinducedintestinalbarrierdysfunction
AT zhenwang plk1protectsagainstsepsisinducedintestinalbarrierdysfunction
AT taoyu plk1protectsagainstsepsisinducedintestinalbarrierdysfunction
AT jingyiwu plk1protectsagainstsepsisinducedintestinalbarrierdysfunction
AT xiaoganjiang plk1protectsagainstsepsisinducedintestinalbarrierdysfunction
AT xiaojujin plk1protectsagainstsepsisinducedintestinalbarrierdysfunction
AT weihualu plk1protectsagainstsepsisinducedintestinalbarrierdysfunction
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