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PLK1 protects intestinal barrier function during sepsis by targeting mitochondrial dynamics through TANK-NF-κB signalling by Ying-Ya Cao; Yuan Zhang; Wuyun Gerile; Yan Guo; Li-Na Wu; Li-Li Wu; Kai Song; Wei-Hua Lu; Jian-Bo Yu is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

What is PLK1 protects intestinal barrier function during sepsis by targeting mitochondrial dynamics through TANK-NF-κB signalling about?

Abstract Background Intestinal barrier integrity in the pathogenesis of sepsis is critical. Despite an abundance of evidence, the molecular mechanism of the intestinal barrier in sepsis pathology remains unclear. Here, we report a protective role of polo-like kinase 1 (PLK1) in intestinal barrier integrity during sepsis. Methods Mice with PLK1 overexpression (CAG-PLK1 mice) or PLK1 inhibition (BI2536-treated mice) underwent caecal ligation and puncture (CLP) to establish a sepsis model. The intestinal barrier function, apoptosis in the intestinal epithelium, mitochondrial function and NF-κB signalling activity were evaluated. To suppress the activation of NF-κB signalling, the NF-κB inhibitor PDTC, was administered. The Caco-2 cell line was chosen to establish an intestinal epithelial injury model in vitro. Results Sepsis destroyed intestinal barrier function, induced excessive apoptosis in the intestinal epithelium, and disrupted the balance of mitochondrial dynamics in wild-type mice. PLK1 overexpression alleviated sepsis-induced damage to the intestinal epithelium by inhibiting the activation of NF-κB signalling. PLK1 colocalized and interacted with TANK in Caco-2 cells. Transfe

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Author
Ying-Ya Cao; Yuan Zhang; Wuyun Gerile; Yan Guo; Li-Na Wu; Li-Li Wu; Kai Song; Wei-Hua Lu; Jian-Bo Yu
Published
2022
Language
EN
Field
Biochemistry, Genetics and Molecular Biology (Life Sciences)

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