scholarly journals S-nitrosylation regulates VE-cadherin phosphorylation and internalization in microvascular permeability

2016 ◽  
Vol 310 (8) ◽  
pp. H1039-H1044 ◽  
Author(s):  
Anita Guequén ◽  
Rodrigo Carrasco ◽  
Patricia Zamorano ◽  
Lorena Rebolledo ◽  
Pia Burboa ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Platelet Activating Factor ◽  
Adherens Junction ◽  
Endothelial Barrier ◽  
Main Element ◽  
Nitric Oxide Production ◽  
Vascular Endothelial ◽  
Junctional Proteins

The adherens junction complex, composed mainly of vascular endothelial (VE)-cadherin, β-catenin, p120, and γ-catenin, is the main element of the endothelial barrier in postcapillary venules. S-nitrosylation of β-catenin and p120 is an important step in proinflammatory agents-induced hyperpermeability. We investigated in vitro and in vivo whether or not VE-cadherin is S-nitrosylated using platelet-activating factor (PAF) as agonist. We report that PAF-stimulates S-nitrosylation of VE-cadherin, which disrupts its association with β-catenin. In addition, based on inhibition of nitric oxide production, our results strongly suggest that S-nitrosylation is required for VE-cadherin phosphorylation on tyrosine and for its internalization. Our results unveil an important mechanism to regulate phosphorylation of junctional proteins in association with S-nitrosylation.

Effects of Periodic Body Acceleration on the In Vivo Vasoactive Response to N-w-nitro–L-arginine and the In Vitro Nitric Oxide Production

2003 ◽  
Vol 31 (11) ◽  
pp. 1337-1346 ◽  
Author(s):  
Jose A. Adams ◽  
James E. Moore, Jr. ◽  
Michael R. Moreno ◽  
Jaqueline Coelho ◽  
Jorge Bassuk ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Production ◽  
Body Acceleration ◽  
Oxide Production

scholarly journals The 12-HHT/BLT2/NO Axis Is Associated to the Wound Healing and Skin Condition in Different Glycaemic States

2019 ◽  
Vol 7 (4) ◽  
pp. 65
Author(s):  
Leguina-Ruzzi ◽  
Ortiz Diban ◽  
Velarde
Keyword(s):  
Nitric Oxide ◽  
Wound Healing ◽  
Tight Junction ◽  
Skin Condition ◽  
Inos Mrna ◽  
Nitric Oxide Production ◽  
Mrna Levels ◽  
Oxide Production

Type 2 diabetes affects over 340 million people worldwide. This condition can go unnoticed and undiagnosed for years, leading to a late stage where high glycaemia produces complications such as delayed wound healing. Studies have shown that 12-HHT through BLT2, accelerates keratinocyte migration and wound healing. Additionally, evidence has shown the role of nitric oxide as a pro-regenerative mediator, which is decreased in diabetes. Our main goal was to study the association between the 12-HHT/BLT2 axis and the nitric oxide production in wound healing under different glycaemia conditions. For that purpose, we used in vivo and in vitro models. Our results show that the skin from diabetic mice showed reduced BLT2 and iNOS mRNA, TEER, 12-HHT, nitrites, and tight junction levels, accompanied by higher MMP9 mRNA levels. Furthermore, a positive correlation between BLT2 mRNA and nitrites was observed. In vitro, HaCaT-BLT2 cells showed higher nitric oxide and tight junction levels, and reduced MMP9 mRNA levels, compared to mock-keratinocytes under low and high glucose condition. The wound healing capacity was associated with higher nitric oxide production and was affected by the NOS inhibition. We suggest that the BLT2 expression improves the keratinocyte response to hyperglycaemia, associated with the production of nitric oxide.

scholarly journals Nitric Oxide Production and Fc Receptor-Mediated Phagocytosis as Functional Readouts of Macrophage Activity upon Stimulation with Inactivated Poultry Vaccines In Vitro

Vaccines ◽  
2020 ◽  
Vol 8 (2) ◽  
pp. 332 ◽  
Author(s):  
Robin van den Biggelaar ◽  
Willem van Eden ◽  
Victor Rutten ◽  
Christine Jansen
Keyword(s):  
Nitric Oxide ◽  
Allantoic Fluid ◽  
Fc Receptor ◽  
Vaccine Antigen ◽  
Nitric Oxide Production ◽  
Oxide Production ◽  
Future Assessment ◽  
Batch Release

Vaccine batches must pass routine quality control to confirm that their ability to induce protection against disease is consistent with batches of proven efficacy from development studies. For poultry vaccines, these tests are often performed in laboratory chickens by vaccination-challenge trials or serological assays. The aim of this study was to investigate innate immune responses against inactivated poultry vaccines and identify candidate immune parameters for in vitro quality tests as alternatives for animal-based quality tests. For this purpose, we set up assays to measure nitric oxide production and phagocytosis by the macrophage-like cell line HD11, upon stimulation with inactivated poultry vaccines for infectious bronchitis virus (IBV), Newcastle disease virus (NDV), and egg drop syndrome virus (EDSV). In both assays, macrophages became activated after stimulation with various toll-like receptor agonists. Inactivated poultry vaccines stimulated HD11 cells to produce nitric oxide due to the presence of mineral oil adjuvant. Moreover, inactivated poultry vaccines were found to enhance Fc receptor-mediated phagocytosis due to the presence of allantoic fluid in the vaccine antigen preparations. We showed that inactivated poultry vaccines stimulated nitric oxide production and Fc receptor-mediated phagocytosis by chicken macrophages. Similar to antigen quantification methods, the cell-based assays described here can be used for future assessment of vaccine batch-to-batch consistency. The ability of the assays to determine the immunopotentiating properties of inactivated poultry vaccines provides an additional step in the replacement of current in vivo batch-release quality tests.

scholarly journals Modulation of Rac1 Activity by ADMA/DDAH Regulates Pulmonary Endothelial Barrier Function

2009 ◽  
Vol 20 (1) ◽  
pp. 33-42 ◽  
Author(s):  
Beata Wojciak-Stothard ◽  
Belen Torondel ◽  
Lan Zhao ◽  
Thomas Renné ◽  
James M. Leiper
Keyword(s):  
Nitric Oxide ◽  
Actin Cytoskeleton ◽  
Barrier Function ◽  
Endothelial Permeability ◽  
Endothelial Barrier ◽  
Endothelial Barrier Function ◽  
Nitric Oxide Synthase Inhibitor ◽  
Rac1 Activity

Endogenously produced nitric oxide synthase inhibitor, asymmetric methylarginine (ADMA) is associated with vascular dysfunction and endothelial leakage. We studied the role of ADMA, and the enzymes metabolizing it, dimethylarginine dimethylaminohydrolases (DDAH) in the regulation of endothelial barrier function in pulmonary macrovascular and microvascular cells in vitro and in lungs of genetically modified heterozygous DDAHI knockout mice in vivo. We show that ADMA increases pulmonary endothelial permeability in vitro and in in vivo and that this effect is mediated by nitric oxide (NO) acting via protein kinase G (PKG) and independent of reactive oxygen species formation. ADMA-induced remodeling of actin cytoskeleton and intercellular adherens junctions results from a decrease in PKG-mediated phosphorylation of vasodilator-stimulated phosphoprotein (VASP) and a subsequent down-regulation of Rac1 activity. The effects of ADMA on endothelial permeability, Rac1 activation and VASP phosphorylation are prevented by overexpression of active DDAHI and DDAHII, whereas inactive DDAH mutants have no effect. These findings demonstrate for the first time that ADMA metabolism critically determines pulmonary endothelial barrier function by modulating Rac1-mediated remodeling of the actin cytoskeleton and intercellular junctions.

Estimating oxygen transport resistance of the microvascular wall

2000 ◽  
Vol 279 (2) ◽  
pp. H657-H671 ◽  
Author(s):  
Arjun Vadapalli ◽  
Roland N. Pittman ◽  
Aleksander S. Popel
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Smooth Muscle ◽  
Diffusion Model ◽  
Oxygen Transport ◽  
Vascular Wall ◽  
Nitric Oxide Production ◽  
Endothelial Surface

The problem of diffusion of O2 across the endothelial surface in precapillary vessels and its utilization in the vascular wall remains unresolved. To establish a relationship between precapillary release of O2 and vascular wall consumption, we estimated the intravascular flux of O2 on the basis of published in vivo measurements. To interpret the data, we utilized a diffusion model of the vascular wall and computed possible physiological ranges for O2 consumption. We found that many flux values were not consistent with the diffusion model. We estimated the mitochondrial-based maximum O2 consumption of the vascular wall (Mmt) and a possible contribution to O2 consumption of nitric oxide production by endothelial cells (MNO). Many values of O2 consumption predicted from the diffusion model exceeded Mmt + MNO. In contrast, reported values of O2consumption for endothelial and smooth muscle cell suspensions and vascular strips in vitro do not exceed Mmt. We conjecture that most of the reported values of intravascular O2 flux are overestimated, and the likely source is in the experimental estimates of convective O2 transport at upstream and downstream points of unbranched vascular segments.

Extract of the seed coat of Tamarindus indica inhibits nitric oxide production by murine macrophages in vitro and in vivo

2004 ◽  
Vol 42 (4) ◽  
pp. 649-658 ◽  
Author(s):  
T. Komutarin ◽  
S. Azadi ◽  
L. Butterworth ◽  
D. Keil ◽  
B. Chitsomboon ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Seed Coat ◽  
Nitric Oxide Production ◽  
Tamarindus Indica ◽  
Murine Macrophages ◽  
Oxide Production
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