In Vitro Topographical Model of Fuchs Dystrophy for Evaluation of Corneal Endothelial Cell Monolayer Formation

2016 ◽  
Vol 5 (22) ◽  
pp. 2896-2910 ◽  
Author(s):  
Muhammad Rizwan ◽  
Gary S. Peh ◽  
Khadijah Adnan ◽  
Sacha L. Naso ◽  
Alon R. Mendez ◽  
...  

2016 ◽  
Vol 5 (22) ◽  
pp. 2960-2960
Author(s):  
Muhammad Rizwan ◽  
Gary S. Peh ◽  
Khadijah Adnan ◽  
Sacha L. Naso ◽  
Alon R. Mendez ◽  
...  


Author(s):  
Fatma Zehra Erkoc‐Biradli ◽  
Alp Ozgun ◽  
Meftune Özgen Öztürk‐Öncel ◽  
Merve Marcali ◽  
Caglar Elbuken ◽  
...  




1994 ◽  
Vol 20 (4) ◽  
pp. 621-628 ◽  
Author(s):  
Paul J. DiMuzio ◽  
Kerri J. Pratt ◽  
Pauline K. Park ◽  
R.Anthony Carabasi


1988 ◽  
Vol 60 (02) ◽  
pp. 240-246 ◽  
Author(s):  
Erna G Langeler ◽  
Victor W M van Hinsbergh

SummaryA model has been developed to study the transport of fluid and macromolecules through human arterial umbilical cord endothelial cell monolayers in vitro. Cells were cultured on fibronectin- coated polycarbonate filters and formed within a few days a tight monolayer, with an electrical resistance of 17 ± 4 Ohm · cm2. The cells were connected by close cell contacts with tight junctions. The passáge-rate of horse radish peroxidase (HRP) through these filters was 20-40 fold lower than through filters without an endothelial monolayer. The continuous presence of 10% human serum was needed to maintain the electrical resistance of the monolayer and its barrier function towards macromolecules. Chelation of extracellular calcium resulted in an increased permeability and a decreased electrical resistance of the monolayer. This process was reversible by re-addition of calcium ions to the cells. The permeation rate of dextrans of various molecular weights (9-480 kD) was inversely related to the molecular mass of the molecule. No difference was measured between the passage rate of dextran of 480 kD and dextran of 2,000 kD. Incubation of the endothelial cell monolayer with 2-deoxy-D-glucose resulted in a decreased permeability but it had no effect on electrical resistance. This suggests that the passage-process is energy- dependent.Fluid permeation through the endothelial cell monolayer on filters was measured in a perfusion chamber under 20 mmHg hydrostatic pressure. It was decreased by the presence of serum proteins and responded reversibly on the chelation and readdition of extracellular calcium ions.



2007 ◽  
Vol 75 (9) ◽  
pp. 4572-4581 ◽  
Author(s):  
E. Behling-Kelly ◽  
David McClenahan ◽  
K. S. Kim ◽  
C. J. Czuprynski

ABSTRACT “Haemophilus somnus” causes thrombotic meningoencephalitis in cattle. Our laboratory has previously reported that H. somnus has the ability to adhere to, but not invade, bovine brain endothelial cells (BBEC) in vitro. The goal of this study was to determine if H. somnus alters brain endothelial cell monolayer integrity in vitro, in a manner that would be expected to contribute to inflammation of the central nervous system (CNS). Monolayer integrity was monitored by measuring transendothelial electrical resistance (TEER) and albumin flux. BBEC incubated with H. somnus underwent rapid cytoskeletal rearrangement, significant increases in albumin flux, and reductions in TEER. Decreased monolayer TEER was preceded by phosphorylation of the myosin regulatory light chain and was partially dependent on tumor necrosis factor alpha and myosin light-chain kinase but not interleukin-1β. Neither heat-killed H. somnus, formalin-fixed H. somnus, nor purified lipooligosaccharide altered monolayer integrity within a 2-h incubation period, whereas conditioned medium from H. somnus-treated BBEC caused a modest reduction in TEER. The data from this study support the hypothesis that viable H. somnus alters integrity of the blood-brain barrier by promoting contraction of BBEC and increasing paracellular permeability of the CNS vasculature.



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