scholarly journals ERG-Associated lncRNA (ERGAL) Promotes the Stability and Integrity of Vascular Endothelial Barrier During Dengue Viral Infection via Interaction With miR-183-5p

2020 ◽  
Vol 10 ◽  
Author(s):  
Baojia Zheng ◽  
Hui Wang ◽  
Guohui Cui ◽  
Qianfang Guo ◽  
Lulu Si ◽  
...  
Keyword(s):  
Viral Infection ◽  
Endothelial Barrier ◽  
Vascular Endothelial ◽  
The Stability

scholarly journals Interfering with VE-PTP stabilizes endothelial junctions in vivo via Tie-2 in the absence of VE-cadherin

2015 ◽  
Vol 212 (13) ◽  
pp. 2267-2287 ◽  
Author(s):  
Maike Frye ◽  
Martina Dierkes ◽  
Verena Küppers ◽  
Matthias Vockel ◽  
Janina Tomm ◽  
...  
Keyword(s):  
Tyrosine Phosphatase ◽  
Endothelial Barrier ◽  
Vascular Endothelial ◽  
Leukocyte Transmigration ◽  
Gene Ablation ◽  
Nonmuscle Myosin Ii ◽  
Endothelial Junctions ◽  
The Stability ◽  
Endothelial Junction

Vascular endothelial (VE)–protein tyrosine phosphatase (PTP) associates with VE-cadherin, thereby supporting its adhesive activity and endothelial junction integrity. VE-PTP also associates with Tie-2, dampening the tyrosine kinase activity of this receptor that can support stabilization of endothelial junctions. Here, we have analyzed how interference with VE-PTP affects the stability of endothelial junctions in vivo. Blocking VE-PTP by antibodies, a specific pharmacological inhibitor (AKB-9778), and gene ablation counteracted vascular leak induction by inflammatory mediators. In addition, leukocyte transmigration through the endothelial barrier was attenuated. Interference with Tie-2 expression in vivo reversed junction-stabilizing effects of AKB-9778 into junction-destabilizing effects. Furthermore, lack of Tie-2 was sufficient to weaken the vessel barrier. Mechanistically, inhibition of VE-PTP stabilized endothelial junctions via Tie-2, which triggered activation of Rap1, which then caused the dissolution of radial stress fibers via Rac1 and suppression of nonmuscle myosin II. Remarkably, VE-cadherin gene ablation did not abolish the junction-stabilizing effect of the VE-PTP inhibitor. Collectively, we conclude that inhibition of VE-PTP stabilizes challenged endothelial junctions in vivo via Tie-2 by a VE-cadherin–independent mechanism. In the absence of Tie-2, however, VE-PTP inhibition destabilizes endothelial barrier integrity in agreement with the VE-cadherin–supportive effect of VE-PTP.

scholarly journals Lipid Raft Association Stabilizes VEGF Receptor 2 in Endothelial Cells

2021 ◽  
Vol 22 (2) ◽  
pp. 798
Author(s):  
Ibukunoluwapo O. Zabroski ◽  
Matthew A. Nugent
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Lipid Rafts ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
Potential Mechanism ◽  
Lysosomal Degradation ◽  
Extracellular Signal ◽  
The Stability ◽  
Endothelial Growth Factor

The binding of vascular endothelial growth factor A (VEGF) to VEGF receptor-2 (VEGFR-2) stimulates angiogenic signaling. Lipid rafts are cholesterol-dense regions of the plasma membrane that serve as an organizational platform for biomolecules. Although VEGFR2 has been shown to colocalize with lipid rafts to regulate its activation, the effect of lipid rafts on non-activated VEGFR2 has not been explored. Here, we characterized the involvement of lipid rafts in modulating the stability of non-activated VEGFR2 in endothelial cells using raft disrupting agents: methyl-β-cyclodextrin, sphingomyelinase and simvastatin. Disrupting lipid rafts selectively decreased the levels of non-activated VEGFR2 as a result of increased lysosomal degradation. The decreased expression of VEGFR2 translated to reduced VEGF-activation of the extracellular signal-regulated protein kinases (ERK). Overall, our results indicate that lipid rafts stabilize VEGFR2 and its associated signal transduction activities required for angiogenesis. Thus, modulation of lipid rafts may provide a means to regulate the sensitivity of endothelial cells to VEGF stimulation. Indeed, the ability of simvastatin to down regulate VEGFR2 and inhibit VEGF activity suggest a potential mechanism underlying the observation that this drug improves outcomes in the treatment of certain cancers.

Stability of a CD4+ T cell viral infection model with diffusion

2018 ◽  
Vol 11 (05) ◽  
pp. 1850071 ◽  
Author(s):  
Zhiting Xu ◽  
Youqing Xu
Keyword(s):  
T Cell ◽  
Viral Infection ◽  
Lyapunov Functions ◽  
Threshold Value ◽  
Endemic Equilibrium ◽  
Infection Model ◽  
Asymptotically Stable ◽  
Globally Asymptotically Stable ◽  
The Stability ◽  
Viral Infection Model

This paper is devoted to the study of the stability of a CD[Formula: see text] T cell viral infection model with diffusion. First, we discuss the well-posedness of the model and the existence of endemic equilibrium. Second, by analyzing the roots of the characteristic equation, we establish the local stability of the virus-free equilibrium. Furthermore, by constructing suitable Lyapunov functions, we show that the virus-free equilibrium is globally asymptotically stable if the threshold value [Formula: see text]; the endemic equilibrium is globally asymptotically stable if [Formula: see text] and [Formula: see text]. Finally, we give an application and numerical simulations to illustrate the main results.

scholarly journals Ethanol Disrupts Vascular Endothelial Barrier: Implication in Cancer Metastasis

2012 ◽  
Vol 127 (1) ◽  
pp. 42-53 ◽  
Author(s):  
Mei Xu ◽  
Gang Chen ◽  
Wei Fu ◽  
Mingjun Liao ◽  
Jacqueline A. Frank ◽  
...  
Keyword(s):  
Cancer Metastasis ◽  
Endothelial Barrier ◽  
Vascular Endothelial
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