scholarly journals Endothelial barrier dysfunction in diabetic conduit arteries: a novel method to quantify filtration

2013 ◽  
Vol 304 (3) ◽  
pp. H398-H405 ◽  
Author(s):  
Xiao Lu ◽  
Virginia H. Huxley ◽  
Ghassan S. Kassab
Keyword(s):  
Pressure Range ◽  
Diabetic Rats ◽  
Endothelial Barrier ◽  
Endothelial Glycocalyx ◽  
Intraluminal Pressure ◽  
Unit Surface Area ◽  
Barrier Dysfunction ◽  
Femoral Arteries ◽  
Adventitial Layer ◽  
User Friendly

The endothelial barrier plays an important role in atherosclerosis, hyperglycemia, and hypercholesterolemia. In the present study, an accurate, reproducible, and user-friendly method was used to further understand endothelial barrier function of conduit arteries. An isovolumic method was used to measure the hydraulic conductivity ( Lp) of the intact vessel wall and medial-adventitial layer. Normal arterial segments with diameters from 0.2 to 5.5 mm were used to validate the method, and femoral arteries of diabetic rats were studied as an example of pathological specimens. Various arterial segments confirmed that the volume flux of water per unit surface area was linearly related to intraluminal pressure, as confirmed in microvessels. Lp of the intact wall varied from 3.5 to 22.1 × 10−7 cm·s−1·cmH2O−1 over the pressure range of 7–180 mmHg. Over the same pressure range, Lp of the endothelial barrier changed from 4.4 to 25.1 × 10−7 cm·s−1·cmH2O−1. During perfusion with albumin-free solution, Lp of rat femoral arteries increased from 6.1 to 13.2 × 10−7 cm·s−1·cmH2O−1 over the pressure range of 10–180 mmHg. Hyperglycemia increased Lp of the femoral artery in diabetic rats from 2.9 to 5.5 × 10−7 cm·s−1·cmH2O−1 over the pressure range of 20–135 mmHg. In conclusion, the Lp of a conduit artery can be accurately and reproducibly measured using a novel isovolumic method, which in diabetic rats is hyperpermeable. This is likely due to disruption of the endothelial glycocalyx.

scholarly journals Changes in endothelial glycocalyx layer protective ability after inflammatory stimulus

2020 ◽  
Author(s):  
Luis F. Delgadillo ◽  
Elena B. Lomakina ◽  
Julia Kuebel ◽  
Richard E. Waugh
Keyword(s):  
Endothelial Cells ◽  
Fluid Transport ◽  
Leukocyte Adhesion ◽  
Umbilical Vein ◽  
Barrier Properties ◽  
Endothelial Barrier ◽  
Endothelial Glycocalyx ◽  
Neutrophil Adhesion ◽  
Barrier Dysfunction ◽  
Endothelial Glycocalyx Layer

Leukocyte adhesion to the endothelium is an important early step in the initiation and progression of sepsis. The endothelial glycocalyx layer (EGL) has been implicated in neutrophil adhesion and barrier dysfunction, but studies in this area are few. In this report we examine the hypothesis that damage to the structure of the EGL caused by inflammation leads to increased leukocyte adhesion and endothelial barrier dysfunction. We used human umbilical vein endothelial cells (HUVECs) enzymatically treated to remove the EGL components hyaluronic acid (HA) and heparan sulfate (HS) as a model for EGL damage. Using atomic force microscopy, we show reductions in EGL thickness after removal of either HA or HS individually, but the largest decrease, comparable to TNF-a treatment, was observed when both HA and HS were removed. Interestingly, removal of HS or HA individually did not affect neutrophil adhesion significantly, but removal of both constituents resulted in increased neutrophil adhesion. To test EGL contributions to endothelial barrier properties, we measured trans-endothelial electrical resistance (TEER) and diffusion of fluorescently labeled dextran (10 kDa MW) across the monolayer. Removal of EGL components decreased TEER, but had an insignificant effect on dextran diffusion rates. The reduction in TEER suggests that disruption of the EGL may predispose endothelial cells to increased rates of fluid leakage. These data support the view that damage to the EGL during inflammation has significant effects on the accessibility of adhesion molecules, likely facilitates leukocyte adhesion, and may also contribute to increased rates of fluid transport into tissues.

scholarly journals Atrial Natriuretic Peptide Protects against Histamine-Induced Endothelial Barrier Dysfunction in Vivo

2008 ◽  
Vol 74 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Robert Fürst ◽  
Martin F. Bubik ◽  
Peter Bihari ◽  
Bettina A. Mayer ◽  
Alexander G. Khandoga ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Endothelial Barrier ◽  
Barrier Dysfunction ◽  
Endothelial Barrier Dysfunction ◽  
Atrial Natriuretic

Effect of p18 on Endothelial Barrier Function by Mediating Vascular Endothelial Rab11a-VE-cadherin Recycling

2021 ◽  
Author(s):  
Bo-Wen Xu ◽  
Zhi-Qiang Cheng ◽  
Xu-Ting Zhi ◽  
Xiao-Mei Yang ◽  
Zhi-Bo Yan
Keyword(s):  
Barrier Function ◽  
Adherens Junctions ◽  
Cecal Ligation ◽  
Underlying Mechanism ◽  
Endothelial Barrier ◽  
Endothelial Barrier Function ◽  
Barrier Dysfunction ◽  
Recycling Endosome

Abstract Endothelial barrier integrity requires recycling of VE-cadherin to adherens junctions. Both p18 and Rab11a play significant roles in VE-cadherin recycling. However, the underlying mechanism and the role of p18 in activating Rab11a have yet to be elucidated. Performing in vitro and in vivo experiments, we showed that p18 protein bound to VE-cadherin before Rab11a through its VE-cadherin-binding domain (aa 1–39). Transendothelial resistance showed that overexpression of p18 promoted the circulation of VE-cadherin to adherens junctions and the recovery of the endothelial barrier. Silencing of p18 caused endothelial barrier dysfunction and prevented Rab11a-positive recycling endosome accumulation in the perinuclear recycling compartments. Furthermore, p18 knockdown in pulmonary microvessels markedly increased vascular leakage in mice challenged with lipopolysaccharide and cecal ligation puncture. This study showed that p18 regulated the pulmonary endothelial barrier function in vitro and in vivo by regulating the binding of Rab11a to VE-cadherin and the activation of Rab11a.

scholarly journals Microtubule destabilization caused by particulate matter contributes to lung endothelial barrier dysfunction and inflammation

2019 ◽  
Vol 53 ◽  
pp. 246-255 ◽  
Author(s):  
Pratap Karki ◽  
Angelo Meliton ◽  
Albert Sitikov ◽  
Yufeng Tian ◽  
Tomomi Ohmura ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Endothelial Barrier ◽  
Barrier Dysfunction ◽  
Endothelial Barrier Dysfunction
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