scholarly journals Toxicity of Deoxynivalenol and Its Acetylated Derivatives on the Intestine: Differential Effects on Morphology, Barrier Function, Tight Junction Proteins, and Mitogen-Activated Protein Kinases

2012 ◽  
Vol 130 (1) ◽  
pp. 180-190 ◽  
Author(s):  
Philippe Pinton ◽  
Dima Tsybulskyy ◽  
Joelma Lucioli ◽  
Joëlle Laffitte ◽  
Patrick Callu ◽  
...  
Keyword(s):  
Tight Junction ◽  
Protein Kinases ◽  
Barrier Function ◽  
Tight Junction Proteins ◽  
Mitogen Activated Protein Kinases ◽  
Differential Effects ◽  
Mitogen Activated Protein ◽  
Junction Proteins

Chronic adrenomedullin treatment improves blood-brain barrier function but has no effects on expression of tight junction proteins

2003 ◽  
pp. 565-568 ◽  
Author(s):  
Bela Kis ◽  
J. A. Snipes ◽  
M. A. Deli ◽  
C. S. Ábrahám ◽  
H. Yamashita ◽  
...  
Keyword(s):  
Tight Junction ◽  
Blood Brain Barrier ◽  
Barrier Function ◽  
Brain Barrier ◽  
Tight Junction Proteins ◽  
Blood Brain ◽  
Junction Proteins

scholarly journals Differential effects of hydrocortisone and TNFα on tight junction proteins in anin vitromodel of the human blood-brain barrier

2008 ◽  
Vol 586 (7) ◽  
pp. 1937-1949 ◽  
Author(s):  
Carola Förster ◽  
Malgorzata Burek ◽  
Ignacio A. Romero ◽  
Babette Weksler ◽  
Pierre-Olivier Couraud ◽  
...  
Keyword(s):  
Tight Junction ◽  
Blood Brain Barrier ◽  
Human Blood ◽  
Brain Barrier ◽  
Tight Junction Proteins ◽  
Differential Effects ◽  
Blood Brain ◽  
Junction Proteins

scholarly journals The role of zinc deficiency in alcohol-induced intestinal barrier dysfunction

2010 ◽  
Vol 298 (5) ◽  
pp. G625-G633 ◽  
Author(s):  
Wei Zhong ◽  
Craig J. McClain ◽  
Matthew Cave ◽  
Y. James Kang ◽  
Zhanxiang Zhou
Keyword(s):  
Oxidative Stress ◽  
Tight Junction ◽  
Zinc Deficiency ◽  
Barrier Function ◽  
Intestinal Barrier ◽  
Alcohol Exposure ◽  
Epithelial Barrier ◽  
Tight Junction Proteins ◽  
Barrier Dysfunction ◽  
Junction Proteins

Disruption of the intestinal barrier is a causal factor in the development of alcoholic endotoxemia and hepatitis. This study was undertaken to determine whether zinc deficiency is related to the deleterious effects of alcohol on the intestinal barrier. Mice were pair fed an alcohol or isocaloric liquid diet for 4 wk, and hepatitis was detected in association with elevated blood endotoxin level. Alcohol exposure significantly increased the permeability of the ileum but did not affect the barrier function of the duodenum or jejunum. Reduction of tight-junction proteins at the ileal epithelium was detected in alcohol-fed mice although alcohol exposure did not cause apparent histopathological changes. Alcohol exposure significantly reduced the ileal zinc concentration in association with accumulation of reactive oxygen species. Caco-2 cell culture demonstrated that alcohol exposure increases the intracellular free zinc because of oxidative stress. Zinc deprivation caused epithelial barrier disruption in association with disassembling of tight junction proteins in the Caco-2 monolayer cells. Furthermore, minor zinc deprivation exaggerated the deleterious effect of alcohol on the epithelial barrier. In conclusion, epithelial barrier dysfunction in the distal small intestine plays an important role in alcohol-induced gut leakiness, and zinc deficiency attributable to oxidative stress may interfere with the intestinal barrier function by a direct action on tight junction proteins or by sensitizing to the effects of alcohol.

scholarly journals Differential effects of claudin-3 and claudin-4 on alveolar epithelial barrier function

2011 ◽  
Vol 301 (1) ◽  
pp. L40-L49 ◽  
Author(s):  
Leslie A. Mitchell ◽  
Christian E. Overgaard ◽  
Christina Ward ◽  
Susan S. Margulies ◽  
Michael Koval
Keyword(s):  
Epithelial Cells ◽  
Tight Junction ◽  
Barrier Function ◽  
Alveolar Epithelium ◽  
Alveolar Epithelial Cells ◽  
Epithelial Barrier ◽  
Tight Junction Proteins ◽  
Epithelial Barrier Function ◽  
Alveolar Epithelial ◽  
Junction Proteins

Alveolar barrier function depends critically on the claudin family tight junction proteins. Of the major claudins expressed by alveolar epithelial cells, claudin (Cldn)-3 and Cldn-4 are the most closely related by amino acid homology, yet they differ dramatically in the pattern of expression. Previously published reports have shown that Cldn-3 is predominantly expressed by type II alveolar epithelial cells; Cldn-4 is expressed throughout the alveolar epithelium and is specifically upregulated in response to acute lung injury. Using primary rat alveolar epithelial cells transduced with yellow fluorescent protein-tagged claudin constructs, we have identified roles for Cldn-3 and Cldn-4 in alveolar epithelial barrier function. Surprisingly, increasing expression of Cldn-3 decreased alveolar epithelial barrier function, as assessed by transepithelial resistance and dye flux measurements. Conversely, increasing Cldn-4 expression improved alveolar epithelial transepithelial resistance compared with control cells. Other alveolar epithelial tight junction proteins were largely unaffected by increased expression of Cldn-3 and Cldn-4. Taken together, these results demonstrate that, in the context of the alveolar epithelium, Cldn-3 and Cldn-4 have different effects on paracellular permeability, despite significant homology in their extracellular loop domains.

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