scholarly journals Effect of High Glucose on Ocular Surface Epithelial Cell Barrier and Tight Junction Proteins

2020 ◽  
Vol 61 (11) ◽  
pp. 3
Author(s):  
Saleh Alfuraih ◽  
Ashley Barbarino ◽  
Christopher Ross ◽  
Kiumars Shamloo ◽  
Vishal Jhanji ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Tight Junction ◽  
High Glucose ◽  
Ocular Surface ◽  
Tight Junction Proteins ◽  
Surface Epithelial Cell ◽  
Junction Proteins

Digestion of epithelial tight junction proteins by the commensal Clostridium perfringens

2013 ◽  
Vol 305 (10) ◽  
pp. G740-G748 ◽  
Author(s):  
Mihaela Pruteanu ◽  
Fergus Shanahan
Keyword(s):  
Epithelial Cell ◽  
Tight Junction ◽  
Clostridium Perfringens ◽  
Culture Supernatant ◽  
Dependent Manner ◽  
Intestinal Epithelial ◽  
Tight Junction Proteins ◽  
Epithelial Tight Junction ◽  
Junction Proteins ◽  
E Cadherin

The enteric microbiota contributes to the pathogenesis of inflammatory bowel disease, but the pathways involved and bacterial participants may vary in different hosts. We previously reported that some components of the human commensal microbiota, particularly Clostridium perfringens ( C. perfringens), have the proteolytic capacity for host matrix degradation and reduce transepithelial resistance. Here, we examined the C. perfringens-derived proteolytic activity against epithelial tight junction proteins using human intestinal epithelial cell lines. We showed that the protein levels of E-cadherin, occludin, and junctional adhesion molecule 1 decrease in colonic cells treated with C. perfringens culture supernatant. E-cadherin ectodomain shedding in C. perfringens-stimulated intestinal epithelial cells was detected with antibodies against the extracellular domain of E-cadherin, and we demonstrate that this process occurs in a time- and dose-dependent manner. In addition, we showed that the filtered sterile culture supernatant of C. perfringens has no cytotoxic activity on the human intestinal cells at the concentrations used in this study. The direct cleavage of E-cadherin by the proteases from the C. perfringens culture supernatant was confirmed by C. perfringens supernatant-induced in vitro degradation of the human recombinant E-cadherin. We conclude that C. perfringens culture supernatant mediates digestion of epithelial cell junctional proteins, which is likely to enable access to the extracellular matrix components by the paracellular pathway.

Intestinal epithelial cell proliferation, apoptosis and expression of tight junction proteins in patients with obstructive jaundice

2010 ◽  
Vol 41 (2) ◽  
pp. 117-125 ◽  
Author(s):  
Stelios F. Assimakopoulos ◽  
Athanassios C. Tsamandas ◽  
Emanuel Louvros ◽  
Constantine E. Vagianos ◽  
Vassiliki N. Nikolopoulou ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Epithelial Cell ◽  
Obstructive Jaundice ◽  
Tight Junction ◽  
Intestinal Epithelial Cell ◽  
Intestinal Epithelial ◽  
Epithelial Cell Proliferation ◽  
Tight Junction Proteins ◽  
Junction Proteins

Secreted bioactive factors fromBifidobacterium infantisenhance epithelial cell barrier function

2008 ◽  
Vol 295 (5) ◽  
pp. G1025-G1034 ◽  
Author(s):  
Julia B. Ewaschuk ◽  
Hugo Diaz ◽  
Liisa Meddings ◽  
Brendan Diederichs ◽  
Andrea Dmytrash ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Tight Junction ◽  
Cell Permeability ◽  
Tight Junction Proteins ◽  
Gut Permeability ◽  
Tnf Α ◽  
Ifn Γ ◽  
The Impact ◽  
Deficient Mice ◽  
Junction Proteins

Live probiotic bacteria are effective in reducing gut permeability and inflammation. We have previously shown that probiotics release peptide bioactive factors that modulate epithelial resistance in vitro. The objectives of this study were to determine the impact of factors released from Bifidobacteria infantis on intestinal epithelial cell permeability and tight junction proteins and to assess whether these factors retain their bioactivity when administered to IL-10-deficient mice. B. infantis conditioned medium (BiCM) was applied to T84 human epithelial cells in the presence and absence of TNF-α and IFN-γ. Transepithelial resistance (TER), tight junction proteins [claudins 1, 2, 3, and 4, zonula occludens (ZO)-1, and occludin] and MAP kinase activity (p38 and ERK) were examined. Acute effects of BiCM on intestinal permeability were assessed in colons from IL-10-deficient mice in Ussing chambers. A separate group of IL-1-deficient mice was treated with BiCM for 4 wk and then assessed for intestinal histological injury, cytokine levels, epithelial permeability, and immune response to bacterial antigens. In T84 cells, BiCM increased TER, decreased claudin-2, and increased ZO-1 and occludin expression. This was associated with enhanced levels of phospho-ERK and decreased levels of phospho-p38. BiCM prevented TNF-α- and IFN-γ-induced drops in TER and rearrangement of tight junction proteins. Inhibition of ERK prevented the BiCM-induced increase in TER and attenuated the protection from TNF-α and IFN-γ. Oral BiCM administration acutely reduced colonic permeability in mice whereas long-term BiCM treatment in IL-10-deficient mice attenuated inflammation, normalized colonic permeability, and decreased colonic and splenic IFN-γ secretion. In conclusion, peptide bioactive factors from B. infantis retain their biological activity in vivo and are effective in normalizing gut permeability and improving disease in an animal model of colitis. The effects of BiCM are mediated in part by changes in MAP kinases and tight junction proteins.

scholarly journals The serine protease-mediated increase in intestinal epithelial barrier function is dependent on occludin and requires an intact tight junction

2016 ◽  
Vol 311 (3) ◽  
pp. G466-G479 ◽  
Author(s):  
Natalie J. Ronaghan ◽  
Judie Shang ◽  
Vadim Iablokov ◽  
Raza Zaheer ◽  
Pina Colarusso ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Tight Junction ◽  
Serine Protease ◽  
Barrier Function ◽  
Serine Proteases ◽  
Cell Fractionation ◽  
Intestinal Epithelial ◽  
Tight Junction Proteins ◽  
Junction Protein ◽  
Junction Proteins

Barrier dysfunction is a characteristic of the inflammatory bowel diseases (IBD), Crohn's disease and ulcerative colitis. Understanding how the tight junction is modified to maintain barrier function may provide avenues for treatment of IBD. We have previously shown that the apical addition of serine proteases to intestinal epithelial cell lines causes a rapid and sustained increase in transepithelial electrical resistance (TER), but the mechanisms are unknown. We hypothesized that serine proteases increase barrier function through trafficking and insertion of tight junction proteins into the membrane, and this could enhance recovery of a disrupted monolayer after calcium switch or cytokine treatment. In the canine epithelial cell line, SCBN, we showed that matriptase, an endogenous serine protease, could potently increase TER. Using detergent solubility-based cell fractionation, we found that neither trypsin nor matriptase treatment changed levels of tight junction proteins at the membrane. In a fast calcium switch assay, serine proteases did not enhance the rate of recovery of the junction. In addition, serine proteases could not reverse barrier disruption induced by IFNγ and TNFα. We knocked down occludin in our cells using siRNA and found this prevented the serine protease-induced increase in TER. Using fluorescence recovery after photobleaching (FRAP), we found serine proteases induce a greater mobile fraction of occludin in the membrane. These data suggest that a functional tight junction is needed for serine proteases to have an effect on TER, and that occludin is a crucial tight junction protein in this mechanism.

scholarly journals miR-Let7A Controls the Cell Death and Tight Junction Density of Brain Endothelial Cells under High Glucose Condition

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Juhyun Song ◽  
So Ra Yoon ◽  
Oh Yoen Kim
Keyword(s):  
Cell Death ◽  
Tight Junction ◽  
High Glucose ◽  
Cell Damage ◽  
Tight Junction Proteins ◽  
Proinflammatory Response ◽  
Nitrite Production ◽  
High Glucose Condition ◽  
Glucose Condition ◽  
Junction Proteins

Hyperglycemia-induced stress in the brain of patients with diabetes triggers the disruption of blood-brain barrier (BBB), leading to diverse neurological diseases including stroke and dementia. Recently, the role of microRNA becomes an interest in the research for deciphering the mechanism of brain endothelial cell damage under hyperglycemia. Therefore, we investigated whether mircoRNA Let7A (miR-Let7A) controls the damage of brain endothelial (bEnd.3) cells against high glucose condition. Cell viability, cell death marker expressions (p-53, Bax, and cleaved poly ADP-ribose polymerase), the loss of tight junction proteins (ZO-1 and claudin-5), proinflammatory response (interleukin-6, tumor necrosis factor-α), inducible nitric oxide synthase, and nitrite production were confirmed using MTT, reverse transcription-PCR, quantitative-PCR, Western blotting, immunofluorescence, and Griess reagent assay. miR-Let7A overexpression significantly prevented cell death and loss of tight junction proteins and attenuated proinflammatory response and nitrite production in the bEnd.3 cells under high glucose condition. Taken together, we suggest that miR-Let7A may attenuate brain endothelial cell damage by controlling cell death signaling, loss of tight junction proteins, and proinflammatory response against high glucose stress. In the future, the manipulation of miR-Let7A may be a novel solution in controlling BBB disruption which leads to the central nervous system diseases.

Expression of tight junction proteins in low and high resistance epithelial cell lines MDCK-C7 and -C11

2001 ◽  
Vol 120 (5) ◽  
pp. A61
Author(s):  
Salah Amasheh ◽  
Noga Meiri ◽  
Alfred H. Gitter ◽  
Joachim Mankertz ◽  
Joerg D. Schulzke
Keyword(s):  
Epithelial Cell ◽  
Tight Junction ◽  
Cell Lines ◽  
High Resistance ◽  
Tight Junction Proteins ◽  
Epithelial Cell Lines ◽  
Junction Proteins
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