Cortisol inhibits NF-κB and MAPK pathways in LPS activated bovine endometrial epithelial cells

Dong, Junsheng; Qu, Yang; Li, Jianji; Cui, Luying; Wang, Yefan; Lin, Jiaqi; Wang, Heng

doi:10.1016/j.intimp.2018.01.021

Cited by 53 publications

(58 citation statements)

References 40 publications

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“…Research showed that inflammatory stimuli is caused by microbial pathogens, such as Gram‐negative bacteria (i.e Escherichia coli ), which are important pathogens of bovine endometritis. Bacterial lipopolysaccharide is the main component of the cell wall of Gram‐negative bacteria (Dong et al, ), and also an important substance to activate the immune response of the body (Morris, Gilliam, & Li, ).…”

Section: Introductionmentioning

confidence: 99%

miR‐488 mediates negative regulation of the AKT/NF‐κB pathway by targeting Rac1 in LPS‐induced inflammation

Liu

Guo

Jiang

et al. 2019

Journal Cellular Physiology

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Endometritis is an inflammatory change in the structure of the endometrium due to various causes and is a common cause of infertility. Studies have confirmed that microRNAs (miRNAs) play a key regulatory role in various inflammatory diseases.However, the miRNA-mediated mechanism of endometrial inflammation induced by lipopolysaccharides (LPS) remains unclear. In this study, real-time quantitative polymerase chain reaction, Western blot analysis, immunofluorescence and Rac family small GTPase 1 (Rac1) interference were used to reveal the overexpression of miR-488 in the LPS-induced bovine uterus, and the effect of protein kinase B κ-light chain enhancement of the nuclear factor-activated B cells (AKT/NF-κB) pathway in intimal epithelial cells. The results showed that the expression of inflammatory cytokines such as interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α in the experimental group was significantly lower than that in the control group when miR-488 was overexpressed. Similar results were observed in the expression levels of p-AKT, p-IKK, and p-p65 proteins. In addition, the dual-luciferase reporter system confirmed that miRNA-488 may directly target the 3′-untranslated region of Rac1. In turn, the expression of Rac1 was inhibited. Moreover, the nuclear translocation of NF-κB was inhibited, and meanwhile, the accumulation of reactive oxygen species (ROS) in the cells was reduced. Thus, we provide basic data for the negative regulation of miR-488 in LPS-induced inflammation by inhibiting ROS production and the AKT/NF-kB pathway in intimal epithelial cells. K E Y W O R D SAKT/NF-κB, endometritis, lipopolysaccharide, miR-488, ROS

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Section: Introductionmentioning

confidence: 99%

miR‐488 mediates negative regulation of the AKT/NF‐κB pathway by targeting Rac1 in LPS‐induced inflammation

Liu

Guo

Jiang

et al. 2019

Journal Cellular Physiology

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“…It has been reported that MEL suppresses the development and progression of tumours through inhibition of the MAPK pathway . A number of studies outlined that the MAPK signalling pathways contain the Ras‐Raf‐ERK or classical pathway, JNK/p38 MAPK and ERK5 MAPK pathways . Studies have previously reported that MEL exerts an inhibitory effect on tumours through the classical and JNK/p38 MAPK pathways .…”

Section: Resultsmentioning

confidence: 99%

Melittin inhibits proliferation, migration and invasion of bladder cancer cells by regulating key genes based on bioinformatics and experimental assays

Yao

Zhang

et al. 2019

J Cellular Molecular Medi

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The antitumour effect of melittin (MEL) has recently attracted considerable attention. Nonetheless, information regarding the functional role of MEL in bladder cancer (BC) is currently limited. Herein, we investigated the effect of MEL on critical module genes identified in BC. In total, 2015 and 4679 differentially expressed genes (DEGs) associated with BC were identified from the GSE31189 set and The Cancer Genome Atlas database, respectively. GSE‐identified DEGs were mapped and analysed using Gene Ontology and Kyoto Encyclopaedia of Genes and Genomes analyses to determine BC‐involved crucial genes and signal pathways. Coupled with protein–protein interaction network and Molecular Complex Detection analyses, Modules 2 and 4 were highlighted in the progression of BC. In in‐vitro experiments, MEL inhibited the proliferation, migration, and invasion of UM‐UC‐3 and 5637 cells. The expression of NRAS, PAK2, EGFR and PAK1 in Module 4—enriched in the MAPK signalling pathway—was significantly reduced after treatment with MEL at concentrations of 4 or 6 μg/mL. Finally, quantitative reverse transcription‐polymerase chain reaction and Western blotting analyses revealed MEL inhibited the expression of genes at the mRNA (ERK1/2, ERK5, JNK and MEK5), protein (ERK5, MEK5, JNK and ERK1/2) and phosphorylation (p‐ERK1/2, p‐JNK, and p‐38) levels. This novel evidence indicates MEL exerts effects on the ERK5‐MAK pathway—a branch of MAPK signalling pathway. Collectively, these findings provide a theoretical basis for MEL application in BC treatment.

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“…Increased mRNA expressions of TLR4 have been reported in LPS-stimulated BEEC by Shen et al [18], Herath et al [9] and Dong et al [17], and in heat-killed E.coli-stimulated BEEC by Chapwanya et al [19]. Similarly, Yang et al showed that heat-killed E.coli activated TLR4 receptor in HEK293 cells.…”

Section: Discussionmentioning

confidence: 89%

“…Increased level of endogenic cortisol level was observed during parturition [16]. Previous study indicated that cortisol inhibited the inflammatory response in LPS-induced BEEC [17]. However, the relationship between cortisol and the endometritis caused by E.coli have not yet been clarified.…”

Section: Introductionmentioning

confidence: 95%

Different effects of cortisol on pro-inflammatory gene expressions of LPS-, heat-killed E.coli-, or live E.coli-stimulated bovine endometrial epithelial cells

Cui

Wang

et al. 2019

Preprint

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Background: Bacterial infections are common in postpartum dairy cows. Cortisol level has been observed to increase in dairy cows during peripartum period, and is associated with the endometrial innate immunity against pathogen like E.coli . However, the mechanism underlying how cortisol regulates E.coli -induced inflammatory response in bovine endometrial epithelial cells (BEEC) remains elusive. Results: Cortisol decreased the expressions of IL1β, IL6, TNF-α, IL8, and TLR4 mRNA in BEEC treated with LPS or heat-killed E.coli , but up-regulated the these gene expressions in BEEC stimulated by live E.coli . Conclusion: Cortisol exerted the anti-inflammation action on LPS- or heat-killed E.coli -stimulated BEEC, but the pro-inflammation action on live E.coli -induced BEEC.

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Cortisol inhibits NF-κB and MAPK pathways in LPS activated bovine endometrial epithelial cells

Cited by 53 publications

References 40 publications

miR‐488 mediates negative regulation of the AKT/NF‐κB pathway by targeting Rac1 in LPS‐induced inflammation

miR‐488 mediates negative regulation of the AKT/NF‐κB pathway by targeting Rac1 in LPS‐induced inflammation

Melittin inhibits proliferation, migration and invasion of bladder cancer cells by regulating key genes based on bioinformatics and experimental assays

Different effects of cortisol on pro-inflammatory gene expressions of LPS-, heat-killed E.coli-, or live E.coli-stimulated bovine endometrial epithelial cells

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