Anticoagulant Potential of Endothelial Cell Membrane Components

1988 ◽  
Vol 18 (4-6) ◽  
pp. 271-306 ◽  
Author(s):  
Klaus T. Preissner
Keyword(s):  
Endothelial Cell ◽  
Cell Membrane ◽  
Membrane Components

Design of bio-molecular interfaces using liquid crystals demonstrating endotoxin interactions with bacterial cell wall components

RSC Advances ◽  
2015 ◽  
Vol 5 (81) ◽  
pp. 66476-66486 ◽  
Author(s):  
Dibyendu Das ◽  
Sumyra Sidiq ◽  
Santanu Kumar Pal
Keyword(s):  
Cell Wall ◽  
Liquid Crystals ◽  
Cell Membrane ◽  
Bacterial Cell ◽  
Bacterial Cell Wall ◽  
Cell Wall Components ◽  
Bacterial Cell Membrane ◽  
Membrane Components ◽  
Wall Components

Liquid crystals offer a promising approach to study and quantify the interactions between different bacterial cell membrane components with endotoxin at an aqueous interface.

scholarly journals Annexin A2 as a target endothelial cell membrane autoantigen in Behçet's disease

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Peng Chen ◽  
Hai Yan ◽  
Yaping Tian ◽  
Yiping Xun ◽  
Lili Shi ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Membrane ◽  
Behçet’S Disease ◽  
Behcet’S Disease ◽  
Behçet's Disease ◽  
Annexin A2 ◽  
Behcet's Disease

Ultrastructural changes of lung capillary endothelium in response to botulinum C2toxin

1997 ◽  
Vol 82 (2) ◽  
pp. 382-388 ◽  
Author(s):  
L. Ermert ◽  
H.-R. Duncker ◽  
H. Brückner ◽  
F. Grimminger ◽  
T. Hansen ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Membrane ◽  
Structural Integrity ◽  
Ultrastructural Changes ◽  
Capillary Endothelium ◽  
High Dose ◽  
Edema Formation ◽  
Endothelial Layer ◽  
Total Weight Gain ◽  
Microfilament System

Ermert, L., H.-R. Duncker, H. Brückner, F. Grimminger, T. Hansen, R. Rössig, K. Aktories, and W. Seeger.Ultrastructural changes of lung capillary endothelium in response to botulinum C2toxin. J. Appl. Physiol. 82(2): 382–388, 1997.—The role of the endothelial cytoskeleton for the structural integrity of the pulmonary gas exchange area was probed with the use of Clostridium botulinumC2toxin. This agent causes selective loss of nonmuscle F-actin. In buffer-perfused rabbit lungs, vascular pressures were kept within physiological ranges. In different groups, low-dose [0.3 (C2,I)/0.6 (C2,II) ng/ml] and high-dose [10 (C2,I)/20 (C2,II) ng/ml] toxin were applicated into the buffer fluid; experiments were terminated after a total weight gain of either 1 or 7.5 g. Electron microscopy revealed extensive attenuations, undulations, and protrusions of the endothelial layer, suggestive of “remodeling” and “flowing” of the cell membrane in low C2toxin-treated lungs accompanied by few disruptions of the endothelial layer and edema formation. In addition, endothelial cells displayed vesiculation and bleb formation. Lungs that were exposed to high-toxin doses displayed marked attenuations of the endothelial layer in addition to large endothelial cell disruptions, which did not include interendothelial junctions. Interestingly, type II epithelial cells displayed fusion of lamellar bodies. Collectively, these data suggest that the actin microfilament system is instrumental in supporting endothelial cell membrane configuration and integrity and maintains the intimal barrier function of the lung microvasculature.

scholarly journals Activation of endothelial NADPH oxidase during normoxic lung ischemia is KATP channel dependent

2005 ◽  
Vol 289 (6) ◽  
pp. L954-L961 ◽  
Author(s):  
Qunwei Zhang ◽  
Ikuo Matsuzaki ◽  
Shampa Chatterjee ◽  
Aron B. Fisher
Keyword(s):  
Endothelial Cells ◽  
Membrane Potential ◽  
Endothelial Cell ◽  
Cell Membrane ◽  
Nadph Oxidase ◽  
Membrane Depolarization ◽  
Fluorescence Probes ◽  
Ros Generation ◽  
Wild Type ◽  
Channel Dependent

Previous studies have shown endothelial cell membrane depolarization and generation of reactive oxygen species (ROS) in endothelial cells with abrupt reduction in shear stress (ischemia). This study evaluated the role of ATP-sensitive potassium (KATP) channels and NADPH oxidase in the ischemic response by using Kir6.2−/− and gp91phox−/− mice. To evaluate ROS generation, we subjected isolated perfused mouse lungs labeled with 2′,7′-dichlorodihydrofluorescein (DCF), hydroethidine (HE), or diphenyl-1-pyrenylphosphine (DPPP) to control perfusion followed by global ischemia. In wild-type C57BL/6J mice, imaging of subpleural endothelial cells showed a time-dependent increase in intensity for all three fluorescence probes with ischemia, which was blocked by preperfusion with cromakalim (a KATP channel agonist) or diphenyleneiodonium (DPI, a flavoprotein inhibitor). Endothelial cell fluorescence with bis-oxonol, a membrane potential probe, increased during lung ischemia indicating cell membrane depolarization. The change in membrane potential with ischemia in lungs of gp91phox−/− mice was similar to wild type, but ROS generation did not occur. Lungs from Kir6.2−/− showed marked attenuation of the change in both membrane potential and ROS production. Thus membrane depolarization during lung ischemia requires the presence of a KATP channel and is required for activation of NADPH oxidase and endothelial ROS generation.

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