Plakoglobin maintains the integrity of vascular endothelial cell junctions and regulates VEGF-induced phosphorylation of VE-cadherin

2017 ◽  
Vol 162 (1) ◽  
pp. 55-62 ◽  
Author(s):  
Fumitaka Muramatsu ◽  
Hiroyasu Kidoya ◽  
Hisamichi Naito ◽  
Yumiko Hayashi ◽  
Tomohiro Iba ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Vascular Endothelial Cell ◽  
Cell Junctions ◽  
Vascular Endothelial

scholarly journals Autoregulatory “Multitasking” at Endothelial Cell Junctions by Junction-Associated Intermittent Lamellipodia Controls Barrier Properties

2021 ◽  
Vol 11 ◽  
Author(s):  
Jochen Seebach ◽  
Nadine Klusmeier ◽  
Hans Schnittler
Keyword(s):  
Endothelial Cell ◽  
Transcriptional Activation ◽  
Plasma Membranes ◽  
Current Knowledge ◽  
Vascular Endothelial Cell ◽  
Barrier Properties ◽  
Cell Junctions ◽  
Local Concentration ◽  
Vascular Endothelial ◽  
Dynamic Regulation

Vascular endothelial cell (EC) junctions are key structures controlling tissue homeostasis in physiology. In the last three decades, excellent studies have addressed many aspects of this complex and highly dynamic regulation, including cell signaling, remodeling processes of the proteins of tight junctions, adherens junctions, and gap junctions, the cytoskeleton, and post-transcriptional modifications, transcriptional activation, and gene silencing. In this dynamic process, vascular endothelial cadherin (VE-cadherin) provides the core structure of EC junctions mediating the physical adhesion of cells as well as the control of barrier function and monolayer integrity via remodeling processes, regulation of protein expression and post-translational modifications. In recent years, research teams have documented locally restricted dynamics of EC junctions in which actin-driven protrusions in plasma membranes play a central role. In this regard, our research group showed that the dynamics of VE-cadherin is driven by small (1–5 μm) actin-mediated protrusions in plasma membranes that, due to this specific function, were named “junction-associated intermittent lamellipodia” (JAIL). JAIL form at overlapping, adjacent cells, and exactly at this site new VE-cadherin interactions occur, leading to new VE-cadherin adhesion sites, a process that restores weak or lost VE-cadherin adhesion. Mechanistically, JAIL formation occurs locally restricted (1–5 μm) and underlies autoregulation in which the local VE-cadherin concentration is an important parameter. A decrease in the local concentration of VE-cadherin stimulates JAIL formation, whereas an increase in the concentration of VE-cadherin blocks it. JAIL mediated VE-cadherin remodeling at the subjunctional level have been shown to be of crucial importance in angiogenesis, wound healing, and changes in permeability during inflammation. The concept of subjunctional regulation of EC junctions is strongly supported by permeability assays, which can be employed to quantify actin-driven subjunctional changes. In this brief review, we summarize and discuss the current knowledge and concepts of subjunctional regulation in the endothelium.

scholarly journals Vascular Endothelial Integrity Affects the Severity of Enterovirus-Mediated Cardiomyopathy

2021 ◽  
Vol 22 (6) ◽  
pp. 3053
Author(s):  
Jin-Ho Park ◽  
Ha-Hyeon Shin ◽  
Hyun-Seung Rhyu ◽  
So-Hee Kim ◽  
Eun-Seok Jeon ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Vascular Permeability ◽  
Germ Line ◽  
Vascular Endothelial Cell ◽  
Cell Junctions ◽  
Blue Dye ◽  
Vascular Endothelial ◽  
Knock Out ◽  
Endothelial Junction

Coxsackievirus and adenovirus receptor (CAR) is present in epithelial and vascular endothelial cell junctions. We have previously shown a hemorrhagic phenotype in germ-line CAR knock-out mouse embryos; we have also found that CAR interacts with ZO-1 and β-catenin. However, the role of CAR in vascular endothelial junction permeability has not been proven. To understand the roles of CAR in the vascular endothelial junctions, we generated endothelium-specific CAR knockout (CAR-eKO) mice. In the absence of CAR, the endothelial cell layer showed an increase in transmembrane electrical resistance (TER, Ω) and coxsackievirus permeability. Evans blue dye and 70 kDa dextran-FITC were delivered by tail vein injection. We observed increased vascular permeability in the hearts of adult CAR-eKO mice compare with wild-type (WT) mice. There was a marked increase in monocyte and macrophage penetration into the peritoneal cavity caused by thioglycolate-induced peritonitis. We found that CAR ablation in endothelial cells was not significantly increased coxsackievirus B3 (CVB3) induced myocarditis in murine model. However, tissue virus titers were significantly higher in CAR-eKO mice compared with WT. Moreover, CVB3 was detected in the brain of CAR-eKO mice. Endothelial CAR deletion affects the expression of major endothelial junction proteins, such as cadherin and platelet endothelial cell adhesion molecule-1 (PECAM-1) in the cultured endothelial cells as well as liver vessel. We suggest that CAR expression is required for normal vascular permeability and endothelial tight junction homeostasis. Furthermore, CVB3 organ penetration and myocarditis severities were dependent on the endothelial CAR level.

Effect of angiotensin(1-7) on the expression of E-selectin induced by angiotensinII and its mechanism in vascular endothelial cell

2010 ◽  
Vol 34 (8) ◽  
pp. S71-S71
Author(s):  
Xiaohui Shen ◽  
Zhi‑Bin Wen ◽  
Na Li ◽  
Qingmei Cheng ◽  
Xiaofan He ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial

Alterations in Vascular Endothelial Cell-related Plasma Proteins In Thalassaemic Patients and their Correlation with Clinical Symptoms

1995 ◽  
Vol 74 (04) ◽  
pp. 1045-1049 ◽  
Author(s):  
P Butthep ◽  
A Bunyaratvej ◽  
Y Funahara ◽  
H Kitaguchi ◽  
S Fucharoen ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Immunosorbent Assay ◽  
Plasma Proteins ◽  
Clinical Symptoms ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial Cell ◽  
Enzyme Linked Immunosorbent Assay ◽  
Vascular Endothelial ◽  
Leg Ulcers

SummaryAn increased level of plasma thrombomodulin (TM) in α- and β- thalassaemia was demonstrated using an enzyme-linked immunosorbent assay (ELISA). Nonsplenectomized patients with β-thalassaemia/ haemoglobin E (BE) had higher levels of TM than splenectomized cases (BE-S). Patients with leg ulcers (BE-LU) were found to have the highest increase in TM level. Appearance of larger platelets in all types of thalassaemic blood was observed indicating an increase in the number of younger platelets. These data indicate that injury of vascular endothelial cells is present in thalassaemic patients.

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