scholarly journals Desmoglein2 Regulates Claudin2 Expression by Sequestering PI-3-Kinase in Intestinal Epithelial Cells

2021 ◽  
Vol 12 ◽  
Author(s):  
Natalie Burkard ◽  
Michael Meir ◽  
Felix Kannapin ◽  
Christoph Otto ◽  
Maximilian Petzke ◽  
...  
Keyword(s):  
Electrical Resistance ◽  
Intestinal Epithelial Cells ◽  
Direct Interaction ◽  
Transepithelial Electrical Resistance ◽  
Intestinal Epithelial ◽  
Intestinal Epithelial Barrier ◽  
Proximity Ligation ◽  
Inflammatory Conditions ◽  
Basal Expression ◽  
Caco2 Cells

Inflammation-induced reduction of intestinal desmosomal cadherin Desmoglein 2 (Dsg2) is linked to changes of tight junctions (TJ) leading to impaired intestinal epithelial barrier (IEB) function by undefined mechanisms. We characterized the interplay between loss of Dsg2 and upregulation of pore-forming TJ protein Claudin2. Intraperitoneal application of Dsg2-stablising Tandem peptide (TP) attenuated impaired IEB function, reduction of Dsg2 and increased Claudin2 in DSS-induced colitis in C57Bl/6 mice. TP blocked loss of Dsg2-mediated adhesion and upregulation of Claudin2 in Caco2 cells challenged with TNFα. In Dsg2-deficient Caco2 cells basal expression of Claudin2 was increased which was paralleled by reduced transepithelial electrical resistance and by augmented phosphorylation of AKTSer473 under basal conditions. Inhibition of phosphoinositid-3-kinase proved that PI-3-kinase/AKT-signaling is critical to upregulate Claudin2. In immunostaining PI-3-kinase dissociated from Dsg2 under inflammatory conditions. Immunoprecipitations and proximity ligation assays confirmed a direct interaction of Dsg2 and PI-3-kinase which was abrogated following TNFα application. In summary, Dsg2 regulates Claudin2 expression by sequestering PI-3-kinase to the cell borders in intestinal epithelium.

scholarly journals 124 Butyric acid and derivatives: In vitro effects on barrier integrity of porcine intestinal epithelial cells quantified by transepithelial electrical resistance

2020 ◽  
Vol 98 (Supplement_4) ◽  
pp. 109-110
Author(s):  
Lauren L Kovanda ◽  
Monika Hejna ◽  
Yanhong Liu
Keyword(s):  
Butyric Acid ◽  
Sodium Butyrate ◽  
Barrier Function ◽  
Electrical Resistance ◽  
Intestinal Epithelial Cells ◽  
Intestinal Barrier ◽  
Transepithelial Electrical Resistance ◽  
Intestinal Barrier Function ◽  
Intestinal Epithelial

Abstract Intestinal barrier function in vitro is quantified by the transepithelial electrical resistance (TEER) across epithelial cell monolayers due to polarization and expression of tight junction proteins. The objective of the current study was to measure the TEER of porcine intestinal epithelial cells (IPEC-J2) treated with butyric acid, sodium butyrate, monobutyrin and tributyrin. MTT assays were performed for each compound to determine cell viability and appropriate treatment doses. Butyric acid and tributyrin treatments were: 0, 0.5, 1, 2, and 4 mM. Monobutyrin and sodium butyrate doses were: 0, 1, 2, 4, 8 mM. Cells were seeded at 5 × 105 cells/mL into 12-well plates on Corning transwell inserts. Cells were cultured for 4 to 5 days (until all wells had TEER close to 1000 Ωcm2) and were then treated with organic acids. Each compound was tested in a randomized complete block design with 10 replicates. TEER was measured in Ωcm2 using a Millicell ERS-2 voltohmmeter at 0 h (before treatment) and at 24, 48, and 72 h post-treatment. All data were analyzed by PROC MIXED of SAS. Butyric acid linearly enhanced (P < 0.001) TEER of IPEC-J2 dose-dependently, with the highest TEER observed at doses of 1 and 2 mM at each time point. Sodium butyrate did not impact TEER at h 24, but linearly increased (P < 0.05) TEER at h 48 and 72. Treatment of monobutyrin linearly improved (P < 0.001) TEER at h 24, 48, and 72, with the highest TEER observed at the dose of 8 mM. Tributyrin had the tendency to improve (P < 0.10) TEER at h 48 and 72 when the highest dose was applied. Results of the current in vitro study indicate that butyric acid and its derivatives may improve intestinal barrier function of pigs, which requires verification in vivo.

scholarly journals Enterococcus faeciumHDRsEf1 Protects the Intestinal Epithelium and Attenuates ETEC-Induced IL-8 Secretion in Enterocytes

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Zhongyuan Tian ◽  
Xiaofang Liu ◽  
Ran Dai ◽  
Yuncai Xiao ◽  
Xiliang Wang ◽  
...  
Keyword(s):  
Electrical Resistance ◽  
Cell Layer ◽  
Intestinal Epithelial Cells ◽  
Intestinal Barrier ◽  
Transepithelial Electrical Resistance ◽  
Therapeutic Interventions ◽  
Intestinal Epithelial ◽  
Cell Free Supernatant ◽  
Positive Effects ◽  
Intestinal Pathogen

The probioticEnterococcus faeciumHDRsEf1 (Ef1) has been shown to have positive effects on piglet diarrhoea, but the mechanism has not yet been elucidated. In this study, using the IPEC-J2 cell line to mimic intestinal epithelial cells and enterotoxigenicEscherichia coli(ETEC) K88ac as a representative intestinal pathogen, the mechanism underlying Ef1 protection against an enteropathogen was investigated. The results demonstrated that Ef1 was effective in displacing K88ac from the IPEC-J2 cell layer. Moreover, Ef1 and its cell-free supernatant (S-Ef1) modulate IL-8 released by IPEC-J2 cells. Ef1 and its cell-free supernatant showed the potential to protect enterocytes from an acute inflammatory response. In addition, Ef1 and its cell-free supernatant increased the transepithelial electrical resistance (TEER) of the enterocyte monolayer, thus strengthening the intestinal barrier against ETEC. These results may contribute to the development of therapeutic interventions using Ef1 in intestinal disorders of piglets.

scholarly journals Protective Effect of QiOne® 2 Pro on Cultured Intestinal Epithelial Cells after Mobile Phone Radiation

2021 ◽  
Vol 9 (3) ◽  
Author(s):  
Peter C Dartsch
Keyword(s):  
Oxidative Stress ◽  
Coherent State ◽  
Mobile Phone ◽  
Electrical Resistance ◽  
Intestinal Epithelial Cells ◽  
Transepithelial Electrical Resistance ◽  
Epithelial Barrier ◽  
Water Molecules ◽  
Intestinal Epithelial ◽  
Mobile Phone Radiation

QiOne® 2 Pro is a specific device which creates a static field that stimulates water molecules to undergo a transition into the coherent state. Since our body consists of about 70 to 85% of water (depending on age), this coherent state of the water molecules might increase the cellular resistance against exogenous reliabilities such as electromagnetic fields. In this study, the protective effect of QiOne® 2 Pro against mobile phone radiation was examined by using the cultured intestinal epithelial cells. Unprotected cells and untreated control cells served as point of reference. The cell regeneration process as well as the integrity of the intestinal epithelial barrier was investigated by measuring the transepithelial electrical resistance. Mobile phone radiation caused a reduced cell regenerative activity by approximately 60%, whereas the values were about 15% for QiOne® 2 Pro protected cells and untreated controls, respectively. Moreover, mobile phone radiation caused a rupture on the epithelial barrier in unprotected cells by cell death caused due to the oxidative stress with a complete loss of morphological integrity on the barrier. In contrast, untreated controls and QiOne® 2 Pro protected cells did not show any morphological change on the cell layers with an epithelial barrier of a 10-fold higher transepithelial electrical resistance than the unprotected cells. Overall the results clearly demonstrate the sensitivity of intestinal barrier against oxidative stress generated by mobile phone radiation. In addition, the results also show that the QiOne® 2 Pro device is able to reduce unwanted cellular effects of mobile phone radiation.

scholarly journals JunD Represses Transcription and Translation of the Tight Junction Protein Zona Occludens-1 Modulating Intestinal Epithelial Barrier Function

2008 ◽  
Vol 19 (9) ◽  
pp. 3701-3712 ◽  
Author(s):  
Jie Chen ◽  
Lan Xiao ◽  
Jaladanki N. Rao ◽  
Tongtong Zou ◽  
Lan Liu ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Tight Junction ◽  
Barrier Function ◽  
Intestinal Epithelial Cells ◽  
Binding Protein ◽  
Mrna Translation ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Intestinal Epithelial Barrier ◽  
Epithelial Barrier Function

The AP-1 transcription factor JunD is highly expressed in intestinal epithelial cells, but its exact role in maintaining the integrity of intestinal epithelial barrier remains unknown. The tight junction (TJ) protein zonula occludens (ZO)-1 links the intracellular domain of TJ-transmembrane proteins occludin, claudins, and junctional adhesion molecules to many cytoplasmic proteins and the actin cytoskeleton and is crucial for assembly of the TJ complex. Here, we show that JunD negatively regulates expression of ZO-1 and is implicated in the regulation of intestinal epithelial barrier function. Increased JunD levels by ectopic overexpression of the junD gene or by depleting cellular polyamines repressed ZO-1 expression and increased epithelial paracellular permeability. JunD regulated ZO-1 expression at the levels of transcription and translation. Transcriptional repression of ZO-1 by JunD was mediated through cAMP response element-binding protein-binding site within its proximal region of the ZO-1-promoter, whereas induced JunD inhibited ZO-1 mRNA translation by enhancing the interaction of the ZO-1 3′-untranslated region with RNA-binding protein T cell-restricted intracellular antigen 1-related protein. These results indicate that JunD is a biological suppressor of ZO-1 expression in intestinal epithelial cells and plays a critical role in maintaining epithelial barrier function.

scholarly journals Tumour Necrosis Factor Superfamily Members in the Pathogenesis of Inflammatory Bowel Disease

2014 ◽  
Vol 2014 ◽  
pp. 1-15 ◽  
Author(s):  
Tomasz J. Ślebioda ◽  
Zbigniew Kmieć
Keyword(s):  
Inflammatory Bowel Disease ◽  
Tumour Necrosis Factor ◽  
Bowel Disease ◽  
Tumour Necrosis ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Intestinal Epithelial Barrier ◽  
Inflammatory Conditions ◽  
Inflammatory Bowel ◽  
Necrosis Factor

Inflammatory bowel disease (IBD) is a group of inflammatory conditions of the gastrointestinal tract of unclear aetiology of which two major forms are Crohn’s disease (CD) and ulcerative colitis (UC). CD and UC are immunologically distinct, although they both result from hyperactivation of proinflammatory pathways in intestines and disruption of intestinal epithelial barrier. Members of the tumour necrosis factor superfamily (TNFSF) are molecules of broad spectrum of activity, including direct disruption of intestinal epithelial barrier integrity and costimulation of proinflammatory functions of lymphocytes. Tumour necrosis factor (TNF) has a well-established pathological role in IBD which also serves as a target in IBD treatment. In this review we discuss the role of TNF and other TNFSF members, notably, TL1A, FasL, LIGHT, TRAIL, and TWEAK, in the pathogenesis of IBD.

scholarly journals Cellular zinc is required for intestinal epithelial barrier maintenance via the regulation of claudin-3 and occludin expression

2016 ◽  
Vol 311 (1) ◽  
pp. G105-G116 ◽  
Author(s):  
Yuka Miyoshi ◽  
Soichi Tanabe ◽  
Takuya Suzuki
Keyword(s):  
Electrical Resistance ◽  
Molecular Mechanisms ◽  
Transepithelial Electrical Resistance ◽  
Surface Proteins ◽  
Pcr Analysis ◽  
Intestinal Epithelial ◽  
Calpain Activity ◽  
Intracellular Zinc ◽  
Cell Functions ◽  
Zinc Depletion

Intracellular zinc is required for a variety of cell functions, but its precise roles in the maintenance of the intestinal tight junction (TJ) barrier remain unclear. The present study investigated the essential roles of intracellular zinc in the preservation of intestinal TJ integrity and the underlying molecular mechanisms. Depletion of intracellular zinc in both intestinal Caco-2 cells and mouse colons through the application of a cell-permeable zinc chelator N, N, N′, N′-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN) induced a disruption of the TJ barrier, as indicated by increased FITC-labeled dextran flux and decreased transepithelial electrical resistance. The TPEN-induced TJ disruption is associated with downregulation of two TJ proteins, occludin and claudin-3. Biotinylation of cell surface proteins revealed that the zinc depletion induced the proteolysis of occludin but not claudin-3. Occludin proteolysis was sensitive to the inhibition of calpain activity, and increased calpain activity was observed in the zinc-depleted cells. Although quantitative PCR analysis and promoter reporter assay have demonstrated that the zinc depletion-induced claudin-3 downregulation occurred at transcriptional levels, a site-directed mutation in the egr1 binding site in the claudin-3 promoter sequence induced loss of both the basal promoter activity and the TPEN-induced decreases. Reduced egr1 expression by a specific siRNA also inhibited claudin-3 expression and transepithelial electrical resistance maintenance in cells. This study shows that intracellular zinc has an essential role in the maintenance of the intestinal epithelial TJ barrier through regulation of occludin proteolysis and claudin-3 transcription.

scholarly journals Application of Measurements of Transepithelial Electrical Resistance of Intestinal Epithelial Cell Monolayers To Evaluate Probiotic Activity

2005 ◽  
Vol 71 (11) ◽  
pp. 7528-7530 ◽  
Author(s):  
Trine Danø Klingberg ◽  
Maja Herold Pedersen ◽  
Avrelija Cencic ◽  
Birgitte Bjørn Budde
Keyword(s):  
Electrical Resistance ◽  
Intestinal Epithelial Cell ◽  
Transepithelial Electrical Resistance ◽  
Intestinal Epithelial ◽  
Lactobacillus Salivarius ◽  
Cell Monolayers ◽  
Epithelial Cell Monolayers ◽  
Probiotic Lactobacilli ◽  
Dose Dependent ◽  
Probiotic Activity

ABSTRACT Among five potentially probiotic lactobacilli investigated, Lactobacillus plantarum MF1298 and Lactobacillus salivarius DC5 showed the highest increase in the transepithelial electrical resistance (TER) of polarized monolayers of Caco-2 cells, and this increase was shown to be dose dependent. Furthermore, preincubation with MF1298 attenuated a decrease in TER induced by Listeria monocytogenes.

Basal expression of copper transporter 1 in intestinal epithelial cells is regulated by hypoxia-inducible factor 2α

FEBS Letters ◽  
2012 ◽  
Vol 586 (16) ◽  
pp. 2423-2427 ◽  
Author(s):  
Katayoun Pourvali ◽  
Pavle Matak ◽  
Gladys O. Latunde-Dada ◽  
Solomis Solomou ◽  
Maria Mastrogiannaki ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Hypoxia Inducible Factor ◽  
Intestinal Epithelial ◽  
Copper Transporter ◽  
Basal Expression ◽  
Copper Transporter 1
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