Butyrate Enhances Intestinal Epithelial Barrier Function via Up-Regulation of Tight Junction Protein Claudin-1 Transcription

2012 ◽  
Vol 57 (12) ◽  
pp. 3126-3135 ◽  
Author(s):  
Hong-Bo Wang ◽  
Peng-Yuan Wang ◽  
Xin Wang ◽  
Yuan-Lian Wan ◽  
Yu-Cun Liu
Keyword(s):  
Tight Junction ◽  
Barrier Function ◽  
Tight Junction Protein ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Intestinal Epithelial Barrier ◽  
Epithelial Barrier Function ◽  
Junction Protein

scholarly journals PHD3 Stabilizes the Tight Junction Protein Occludin and Protects Intestinal Epithelial Barrier Function

2015 ◽  
Vol 290 (33) ◽  
pp. 20580-20589 ◽  
Author(s):  
Ying Chen ◽  
Hai-Sheng Zhang ◽  
Guo-Hua Fong ◽  
Qiu-Lei Xi ◽  
Guo-Hao Wu ◽  
...  
Keyword(s):  
Tight Junction ◽  
Barrier Function ◽  
Tight Junction Protein ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Intestinal Epithelial Barrier ◽  
Epithelial Barrier Function ◽  
Junction Protein

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 Acidic Bile Salt Modulates the Squamous Epithelial Barrier Function by Modulating Tight Junction Protein

2011 ◽  
Vol 140 (5) ◽  
pp. S-619-S-620
Author(s):  
Xin Chen ◽  
Tadayuki Oshima ◽  
Toshihiko Tomita ◽  
Hirokazu Fukui ◽  
Jiro Watari ◽  
...  
Keyword(s):  
Tight Junction ◽  
Bile Salt ◽  
Barrier Function ◽  
Tight Junction Protein ◽  
Epithelial Barrier ◽  
Epithelial Barrier Function ◽  
Junction Protein

scholarly journals Diesel Exhaust Particle Exposure Reduces Expression of the Epithelial Tight Junction Protein Tricellulin

2020 ◽  
Author(s):  
Timothy Smyth ◽  
Janelle Veazey ◽  
Sophia Eliseeva ◽  
David Chalupa ◽  
Alison Elder ◽  
...  
Keyword(s):  
Tight Junction ◽  
Diesel Exhaust ◽  
Barrier Function ◽  
Diesel Exhaust Particles ◽  
Tight Junction Protein ◽  
Epithelial Barrier ◽  
Airway Epithelial ◽  
Epithelial Barrier Function ◽  
Barrier Integrity ◽  
Junction Protein

Abstract Background: While exposure to diesel exhaust particles has been linked to aberrant immune responses in allergic diseases such as asthma, little attention has been paid to their effects on the airway epithelium. In this study, we sought to determine the effect of diesel exhaust exposure on airway epithelial barrier function and composition using in vitro and in vivo model systems. Methods: 16HBE14o- human bronchial epithelial cells were grown on collagen coated Transwell inserts and exposed to 5 to 50 µg/cm2 SRM 2975 diesel particulate matter (DEP) suspended in cell culture medium or vehicle controls. Changes in barrier function were assessed by measuring transepithelial electrical resistance (TEER) and permeability to 4 kDa FITC Dextran. Neonatal BALB/c mice were exposed to aerosolized DEP (255 ± 89 µg/m3; 2 hours per day for 5 days) and changes in the tight junction protein Tricellulin were assessed two weeks post exposure. Results: A six-hour incubation of epithelial cells with diesel exhaust particles caused a significant concentration-dependent reduction in epithelial barrier integrity as measured by decreased TEER and increased permeability to 4 kDa FITC-Dextran. This reduction in epithelial barrier integrity corresponded to a significant reduction in expression of the tight junction protein Tricellulin. siRNA mediated knockdown of Tricellulin recapitulated changes in barrier function caused by DEP exposure. Neonatal exposure to aerosolized DEP caused a significant reduction in lung Tricellulin two weeks post exposure at both the protein and mRNA level. Conclusion: Short term exposure to DEP causes a significant reduction in epithelial barrier integrity through a reduction in the tight junction protein Tricellulin. Neonatal exposure to aerosolized DEP caused a significant and sustained reduction in Tricellulin protein and mRNA in the lung, suggesting that early life exposure to inhaled DEP may cause lasting changes in airway epithelial barrier function.

scholarly journals Diesel Exhaust Particle Exposure Reduces Expression of the Epithelial Tight Junction Protein Tricellulin

2020 ◽  
Author(s):  
Timothy Smyth ◽  
Janelle Veazey ◽  
Sophia Eliseeva ◽  
David Chalupa ◽  
Alison Elder ◽  
...  
Keyword(s):  
Tight Junction ◽  
Diesel Exhaust ◽  
Barrier Function ◽  
Diesel Exhaust Particles ◽  
Tight Junction Protein ◽  
Epithelial Barrier ◽  
Airway Epithelial ◽  
Epithelial Barrier Function ◽  
Barrier Integrity ◽  
Junction Protein

Abstract Background While exposure to diesel exhaust particles has been linked to aberrant immune responses in allergic diseases such as asthma, little attention has been payed to their effects on the airway epithelium. In this study, we sought to determine the effect of diesel exhaust exposure on airway epithelial barrier function and composition using in vitro and in vivo model systems. 16HBE14o- human bronchial epithelial cells were grown on collagen coated Transwell inserts and exposed to 5 to 50 µg/cm2 SRM 2975 diesel particulate matter (DEP) suspended in cell culture medium or vehicle controls. Changes in barrier function were assessed by measuring transepithelial electrical resistance (TEER) and permeability to 4 kDa FITC Dextran. Neonatal BALB/c mice were exposed to aerosolized DEP (255 ± 89 µg/m3; 2 hours per day for 5 days) and changes in the tight junction protein Tricellulin were assessed two weeks post exposure. Results A six-hour incubation of epithelial cells with diesel exhaust particles caused a significant concentration-dependent reduction in epithelial barrier integrity as measured by decreased TEER and increased permeability to 4 kDa FITC-Dextran. This reduction in epithelial barrier integrity corresponded to a significant reduction in expression of the tight junction protein Tricellulin. siRNA mediated knockdown of Tricellulin recapitulated changes in barrier function caused by DEP exposure. Neonatal exposure to aerosolized DEP caused a significant reduction in lung Tricellulin two weeks post exposure at both the protein and mRNA level. Conclusion Short term exposure to DEP causes a significant reduction in epithelial barrier integrity through a reduction in the tight junction protein Tricellulin. Neonatal exposure to aerosolized DEP caused a significant and sustained reduction in Tricellulin protein and mRNA in the lung, suggesting that early life exposure to inhaled DEP may cause lasting changes in airway epithelial barrier function.

scholarly journals Diesel exhaust particle exposure reduces expression of the epithelial tight junction protein Tricellulin

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Timothy Smyth ◽  
Janelle Veazey ◽  
Sophia Eliseeva ◽  
David Chalupa ◽  
Alison Elder ◽  
...  
Keyword(s):  
Tight Junction ◽  
Diesel Exhaust ◽  
Barrier Function ◽  
Diesel Exhaust Particles ◽  
Tight Junction Protein ◽  
Epithelial Barrier ◽  
Airway Epithelial ◽  
Epithelial Barrier Function ◽  
Barrier Integrity ◽  
Junction Protein

Abstract Background While exposure to diesel exhaust particles has been linked to aberrant immune responses in allergic diseases such as asthma, little attention has been paid to their effects on the airway epithelial barrier. In this study, we sought to determine the effect of diesel exhaust exposure on airway epithelial barrier function and composition using in vitro and in vivo model systems. Methods 16HBE14o- human bronchial epithelial cells were grown on collagen coated Transwell inserts and exposed to 5 to 50 μg/cm2 SRM 2975 diesel particulate matter (DEP) suspended in cell culture medium or vehicle controls. Changes in barrier function were assessed by measuring transepithelial electrical resistance (TEER) and permeability to 4 kDa FITC Dextran. Neonatal BALB/c mice were exposed to aerosolized DEP (255 ± 89 μg/m3; 2 h per day for 5 days) and changes in the tight junction protein Tricellulin were assessed 2 weeks post exposure. Results A six-hour incubation of epithelial cells with diesel exhaust particles caused a significant concentration-dependent reduction in epithelial barrier integrity as measured by decreased TEER and increased permeability to 4 kDa FITC-Dextran. This reduction in epithelial barrier integrity corresponded to a significant reduction in expression of the tight junction protein Tricellulin. siRNA mediated knockdown of Tricellulin recapitulated changes in barrier function caused by DEP exposure. Neonatal exposure to aerosolized DEP caused a significant reduction in lung Tricellulin 2 weeks post exposure at both the protein and mRNA level. Conclusion Short term exposure to DEP causes a significant reduction in epithelial barrier integrity through a reduction in the tight junction protein Tricellulin. Neonatal exposure to aerosolized DEP caused a significant and sustained reduction in Tricellulin protein and mRNA in the lung, suggesting that early life exposure to inhaled DEP may cause lasting changes in airway epithelial barrier function.

scholarly journals Cryptosporidium parvumdisrupts intestinal epithelial barrier function via altering expression of key tight junction and adherens junction proteins

2018 ◽  
Vol 20 (6) ◽  
pp. e12830 ◽  
Author(s):  
Anoop Kumar ◽  
Ishita Chatterjee ◽  
Arivarasu N. Anbazhagan ◽  
Dulari Jayawardena ◽  
Shubha Priyamvada ◽  
...  
Keyword(s):  
Tight Junction ◽  
Barrier Function ◽  
Adherens Junction ◽  
Epithelial Barrier ◽  
Intestinal Epithelial ◽  
Intestinal Epithelial Barrier ◽  
Epithelial Barrier Function ◽  
Adherens Junction Proteins ◽  
Junction Proteins
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