Interleukin-1β Mediates β-Catenin-Driven Downregulation of Claudin-3 and Barrier Dysfunction in Caco2 Cells

Haines, Ricci J.; Beard, Richard S.; Chen, L.; Eitnier, Rebecca A.; Wu, Mack H.

doi:10.1007/s10620-016-4145-y

Cited by 26 publications

(24 citation statements)

References 35 publications

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“…Garcia-Hernandez et al (47), found that claudin-3 was expressed at lower levels in inflammatory bowel disease. Haines et al (19), found that the protein expression levels of claudin-3 were positively correlated with intestinal epithelial tightness. In the present study, immunohistochemistry, western blotting and RT-qPCR were used to analyse the expression profile of claudin-3 in intestinal tissues.…”

Section: Discussionmentioning

confidence: 99%

“…However, there is still no evidence showing the mechanism of action by which emodin protects the intestinal epithelial barrier integrity during sepsis. Since the integrity of the intestinal epithelial barrier is predominantly maintained by intestinal epithelial TJs, the mechanism by which the intestinal epithelial barrier can be improved has been a focus of research (19). Various TJ proteins are expressed differently in intestinal tissue.…”

Section: Introductionmentioning

confidence: 99%

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Protective effect of emodin on intestinal epithelial tight junction barrier integrity in rats with sepsis induced by cecal ligation and puncture

Guo

Zhang

et al. 2020

Exp Ther Med

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Αbstract. The present study investigated the protective effects of emodin on intestinal epithelial tight junction (TJ) barrier integrity in cecal ligation and puncture (CLP)-induced septic rats and its possible mechanisms of action. Healthy male Sprague-Dawley rats were randomly divided into three groups (n=20 per group): Sham group, CLP group and CLP + emodin group. Animals were sacrificed at 12 and 24 h after the model was established. Abdominal aortic blood and specimens of the ileum were harvested for analysis. The histopathological changes in intestinal mucosa and the ultrastructures of intestinal epithelial cells were investigated using light microscopy and transmission electron microscopy. The integrity of the intestinal barrier was assessed by examining plasma diamine oxidase (DAO) levels and the ratio of urine lactulose to mannitol (L/M). The levels of the intestinal TJ proteins claudin-3, zonula occludens (ZO)-1 and occludin were detected using immunohistochemistry, western blotting and reverse transcription-quantitative PCR. The results showed that the pathological damage to intestinal mucosa and the intestinal tissue injury score in the CLP + emodin group were significantly reduced compared to those of the CLP group, and the differences were more obvious at 24 h compared with 12 h. DAO activity and the L/M ratio in the emodin pre-treatment group decreased significantly at 24 h compared with the CLP groups. The protein and mRNA levels of the TJ proteins claudin-3, ZO-1 and occludin in the emodin pre-treatment groups at 12 and 24 h were increased, while occludin mRNA level was found to be decreased compared with the CLP groups. The present study suggested that emodin may significantly reduce the damage to the intestinal epithelial barrier in sepsis, inhibit intestinal barrier permeability and protect intestinal barrier integrity. Emodin may protect intestinal barrier integrity by elevating expression levels of the TJ proteins claudin-3, ZO-1 and occludin in CLP rats.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Protective effect of emodin on intestinal epithelial tight junction barrier integrity in rats with sepsis induced by cecal ligation and puncture

Guo

Zhang

et al. 2020

Exp Ther Med

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“…Published data have shown a number of factors that are associated with the Tj abnormality-associated epithelial barrier dysfunction. Exposure to proinflammatory cytokine, such as IL-1β, can inhibit the expression of claudin-3 in intestinal epithelial cells [ 26 ]. Our data have added novel evidence to this point by showing that VitD deficiency is one of the causative factors of epithelial barrier dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Vitamin D3 induces vitamin D receptor and HDAC11 binding to relieve the promoter of the tight junction proteins

et al. 2017

Oncotarget

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Intestinal epithelial barrier dysfunction and vitamin D (VitD)-deficiency play a critical role in a large number of diseases. The histone deacetylases (HDAC) are associated with a large number of immune diseases. This study tests a hypothesis that the interaction between VitD and HDAC is associated with the regulation of epithelial barrier functions. In this study, human intestinal epithelial cell line, T84 cells, was cultured into monolayers to be used as a model to test the epithelial barrier functions. We observed that in a VitD-deficient environment, the T84 monolayer barrier function was compromised. Exposure to calcitriol (the active form of VitD3) in the culture increased the expression of VitD receptor (VDR) in T84 cells. In a VitD-sufficient environment, VDR formed a complex with histone deacetylase-11 (HDAC11); the complex was markedly decreased in a VitD-deficient environment. We also observed that significantly more binding of HDAC11 to the promoter of the tight junction proteins inhibit the gene transcription activities of these loci in the VitD-deficient environment, which were abolished by the presence of calcitriol in the culture. In conclusion, the interaction between VDR and HDAC11 plays a crucial role in the maintenance of the epithelial barrier integrity.

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“…Evidence suggest that induction of different miRs can be responsible for the decreased expression of intestinal epithelial claudins during mucosal inflammation. Specifically, miR-29 suppresses claudin-1 level [78], miR-93 inhibits claudin-3 [71], and miR-223 downregulates claudin-8 expression [73]. Of note, claudins are not the only targets for different miRs at epithelial junctions, since this mechanism was also implicated in the expressional regulation of occludin and ZO-1 [79, 80].…”

Section: Regulation Of Aj and Tj Protein Expression In Inflamed Inmentioning

confidence: 99%

Disruption of the epithelial barrier during intestinal inflammation: Quest for new molecules and mechanisms

Lechuga

Ivanov

2017

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

199

164

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The intestinal epithelium forms a key protective barrier that separates internal organs from the harmful environment of the gut lumen. Increased permeability of the gut barrier is a common manifestation of different inflammatory disorders contributing to the severity of disease. Barrier permeability is controlled by epithelial adherens junctions and tight junctions. Junctional assembly and integrity depend on fundamental homeostatic processes such as cell differentiation, rearrangements of the cytoskeleton, and vesicle trafficking. Alterations of intestinal epithelial homeostasis during mucosal inflammation may impair structure and remodeling of apical junctions, resulting in increased permeability of the gut barrier. In this review, we summarize recent advances in our understanding of how altered epithelial homeostasis affects the structure and function of adherens junctions and tight junctions in the inflamed gut. Specifically, we focus on the transcription reprogramming of the cell, alterations in the actin cytoskeleton, and junctional endocytosis and exocytosis. We pay special attention to knockout mouse model studies and discuss the relevance of these mechanisms to human gastrointestinal disorders.

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Interleukin-1β Mediates β-Catenin-Driven Downregulation of Claudin-3 and Barrier Dysfunction in Caco2 Cells

Cited by 26 publications

References 35 publications

Protective effect of emodin on intestinal epithelial tight junction barrier integrity in rats with sepsis induced by cecal ligation and puncture

Protective effect of emodin on intestinal epithelial tight junction barrier integrity in rats with sepsis induced by cecal ligation and puncture

Vitamin D3 induces vitamin D receptor and HDAC11 binding to relieve the promoter of the tight junction proteins

Disruption of the epithelial barrier during intestinal inflammation: Quest for new molecules and mechanisms

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