Modulation of Endothelial Paracellular Permeability

1992 ◽  
pp. 103-126 ◽  
Author(s):  
F. R. Haselton ◽  
J. S. Alexander ◽  
S. N. Mueller ◽  
A. P. Fishman
Keyword(s):  
Paracellular Permeability

The protective effect of rebamipide on paracellular permeability of rat gastric epithelial cells

2003 ◽  
Vol 18 ◽  
pp. 133-138 ◽  
Author(s):  
T. Joh ◽  
Y. Takezono ◽  
T. Oshima ◽  
M. Sasaki ◽  
K. Seno ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Protective Effect ◽  
Paracellular Permeability ◽  
Gastric Epithelial Cells

The toxin of diarrheic shellfish poisoning, okadaic acid, increases intestinal epithelial paracellular permeability

1997 ◽  
Vol 112 (1) ◽  
pp. 100-108 ◽  
Author(s):  
J Tripuraneni ◽  
A Koutsouris ◽  
L Pestic ◽  
P De Lanerolle ◽  
G Hecht
Keyword(s):  
Okadaic Acid ◽  
Paracellular Permeability ◽  
Intestinal Epithelial ◽  
Shellfish Poisoning ◽  
Diarrheic Shellfish Poisoning

Effect of short-chain fatty acids on paracellular permeability in Caco-2 intestinal epithelium model

1997 ◽  
Vol 272 (4) ◽  
pp. G705-G712 ◽  
Author(s):  
J. M. Mariadason ◽  
D. H. Barkla ◽  
P. R. Gibson
Keyword(s):  
Fatty Acids ◽  
Cell Line ◽  
Antigen Expression ◽  
Short Chain Fatty Acids ◽  
Paracellular Permeability ◽  
Short Chain ◽  
Differentiating Agents ◽  
The Relationship ◽  
Chain Fatty Acids

Control of paracellular permeability in the colonic epithelium is fundamental to its functional competence. This study examines the relationship between physiologically relevant short-chain fatty acids (SCFAs) and paracellular permeability using the Caco-2 cell line model. Butyrate induced a concentration-dependent, reversible increase in transepithelial resistance (TER) that was maximal after 72 h. Butyrate (2 mM) increased TER by 299 +/- 69% (mean +/- SE; n = 5; P < 0.05; t-test) and reduced mannitol flux to 52 +/- 11% (P < 0.05) of control. The effect of butyrate was dependent on protein synthesis and gene transcription but not dependent on its oxidation or activation of adenosine 3',5'-cyclic monophosphate. The other SCFAs, propionate and acetate, also induced a concentration-dependent increase in TER. The effect of butyrate paralleled changes in cellular differentiation, because alkaline phosphatase activity, carcinoembryonic antigen expression, and dome formation were increased. Furthermore, other differentiating agents (dimethyl sulfoxide and retinoic acid) also increased TER. Thus SCFAs reduce paracellular permeability in the Caco-2 cell line, possibly by promotion of a more differentiated phenotype. If such an effect occurs in vivo, it may have ramifications for the biology and pathobiology of colonic mucosa.

scholarly journals Effect of Lactobacilli on Paracellular Permeability in the Gut

Nutrients ◽  
2011 ◽  
Vol 3 (1) ◽  
pp. 104-117 ◽  
Author(s):  
Siv Ahrne ◽  
Marie-Louise Johansson Hagslatt
Keyword(s):  
Paracellular Permeability

Secretin regulates paracellular permeability in canine gastric monolayers by a Src kinase-dependent pathway

2002 ◽  
Vol 283 (4) ◽  
pp. G893-G899 ◽  
Author(s):  
Monica C. Chen ◽  
Travis E. Solomon ◽  
Eduardo Perez Salazar ◽  
Robert Kui ◽  
Enrique Rozengurt ◽  
...  
Keyword(s):  
Gastric Mucosa ◽  
Epithelial Cells ◽  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitor ◽  
Tyrosine Phosphorylation ◽  
Molecular Mechanisms ◽  
Kinase Inhibitor ◽  
Paracellular Permeability ◽  
Maximal Response ◽  
Src Tyrosine Kinase

Previous studies found that epidermal growth factor (EGF) decreased paracellular permeability in gastric mucosa, but the other physiological regulators and the molecular mechanisms mediating these responses remain undefined. We investigated the role of secretin and Src in regulating paracellular permeability because secretin regulates gastric chief cell function and Src mediates events involving the cytoskeletal-membrane interface, respectively. Confluent monolayers were formed from canine gastric epithelial cells in short-term culture on Transwell filter inserts. Resistance was monitored in the presence of secretin with or without specific kinase inhibitors. Tyrosine phosphorylation of Src at Tyr416 was measured with a site-specific phosphotyrosine antibody. Basolateral, but not apical, secretin at concentrations from 1 to 100 nM dose dependently increased resistance; this response was rapid and sustained over hours. PP2 (10 μM), a selective Src tyrosine kinase inhibitor, but not the inactive isomer PP3, abolished the increase in resistance by secretin but only modestly attenuated apical EGF effects. AG-1478 (100 nM), a specific EGF receptor tyrosine kinase inhibitor, attenuated the resistance increase to EGF but not secretin. Secretin, but not EGF, induced tyrosine phosphorylation of Src at Tyr416 in a dose-dependent fashion, with the maximal response observed at 1 min. PP2, but not PP3, dramatically inhibited this tyrosine phosphorylation. Secretin increases paracellular resistance in gastric mucosa through a Src-mediated pathway, while the effect of EGF is Src independent. Src appears to mediate the physiological effects of this Gs-coupled receptor in primary epithelial cells.

scholarly journals Interaction between Epithelial Sodium Channel γ-Subunit and Claudin-8 Modulates Paracellular Sodium Permeability in Renal Collecting Duct

2020 ◽  
Vol 31 (5) ◽  
pp. 1009-1023 ◽  
Author(s):  
Ali Sassi ◽  
Yubao Wang ◽  
Alexandra Chassot ◽  
Olga Komarynets ◽  
Isabelle Roth ◽  
...  
Keyword(s):  
Sodium Channel ◽  
Knockout Mice ◽  
Collecting Duct ◽  
Epithelial Sodium Channel ◽  
Paracellular Permeability ◽  
Sodium Reabsorption ◽  
Kidney Tubule ◽  
Sodium Permeability ◽  
Tubular Lumen ◽  
Renal Collecting Duct

BackgroundWater and solute transport across epithelia can occur via the transcellular or paracellular pathways. Tight junctions play a key role in mediating paracellular ion reabsorption in the kidney. In the renal collecting duct, which is a typical absorptive tight epithelium, coordination between transcellular sodium reabsorption and paracellular permeability may prevent the backflow of reabsorbed sodium to the tubular lumen along a steep electrochemical gradient.MethodsTo investigate whether transcellular sodium transport controls tight-junction composition and paracellular permeability via modulating expression of the transmembrane protein claudin-8, we used cultured mouse cortical collecting duct cells to see how overexpression or silencing of epithelial sodium channel (ENaC) subunits and claudin-8 affect paracellular permeability. We also used conditional kidney tubule–specific knockout mice lacking ENaC subunits to assess the ENaC’s effect on claudin-8 expression.ResultsOverexpression or silencing of the ENaC γ-subunit was associated with parallel and specific changes in claudin-8 abundance. Increased claudin-8 abundance was associated with a reduction in paracellular permeability to sodium, whereas decreased claudin-8 abundance was associated with the opposite effect. Claudin-8 overexpression and silencing reproduced these functional effects on paracellular ion permeability. Conditional kidney tubule–specific ENaC γ-subunit knockout mice displayed decreased claudin-8 expression, confirming the cell culture experiments' findings. Importantly, ENaC β-subunit or α-subunit silencing or kidney tubule–specific β-ENaC or α-ENaC knockout mice did not alter claudin-8 abundance.ConclusionsOur data reveal the specific coupling between ENaC γ-subunit and claudin-8 expression. This coupling may play an important role in preventing the backflow of reabsorbed solutes and water to the tubular lumen, as well as in coupling paracellular and transcellular sodium permeability.

Perfluorohexadecanoic acid increases paracellular permeability in endothelial cells through the activation of plasma kallikrein-kinin system

Chemosphere ◽  
2018 ◽  
Vol 190 ◽  
pp. 191-200 ◽  
Author(s):  
Qian S. Liu ◽  
Fang Hao ◽  
Zhendong Sun ◽  
Yanmin Long ◽  
Qunfang Zhou ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Paracellular Permeability ◽  
Plasma Kallikrein ◽  
Kinin System ◽  
Kallikrein Kinin System
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