PLK1 protects against sepsis-induced intestinal barrier dysfunction.

PLK1 protects against sepsis-induced intestinal barrier dysfunction.
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PLK1可预防败血症引起的肠屏障功能障碍。

DOI:
10.1038/s41598-018-19573-x
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发表时间:
2018-01-18
期刊:
影响因子:
4.6
通讯作者:
Lu W
Lu W
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Cao Y;Chen Q;Wang Z;Yu T;Wu J;Jiang X;Jin X;Lu W

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脓毒症和脓毒症相关的肠道屏障功能障碍在重症监护病房中很常见,死亡率很高。本研究的目的是调查 Polo 样激酶 1 (PLK1) 是否可以改善脓毒症引起的肠上皮肠屏障功能障碍。注射脂多糖(LPS)后,由于肠上皮细胞凋亡和增殖抑制,小鼠肠道屏障遭到破坏,并伴有PLK1下降。在HT-29肠上皮细胞中,LPS刺激诱导细胞凋亡并抑制细胞增殖。 PLK1的过表达部分挽救了LPS引起的HT29细胞的凋亡和增殖抑制。最后,LPS刺激促进PLK1减少,导致肠上皮细胞凋亡和增殖抑制,破坏肠上皮屏障。这些发现表明 PLK1 可能是治疗脓毒症引起的肠道屏障功能障碍的潜在治疗靶点。
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.
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