Faculty Opinions recommendation of Leukocyte extravasation and vascular permeability are each controlled in vivo by different tyrosine residues of VE-cadherin.

2014 ◽  
Author(s):  
William A Muller
Keyword(s):  
Vascular Permeability ◽  
Tyrosine Residues ◽  
Leukocyte Extravasation

Leukocyte extravasation and vascular permeability are each controlled in vivo by different tyrosine residues of VE-cadherin

2014 ◽  
Vol 15 (3) ◽  
pp. 223-230 ◽  
Author(s):  
Florian Wessel ◽  
Mark Winderlich ◽  
Maren Holm ◽  
Maike Frye ◽  
Ronmy Rivera-Galdos ◽  
...  
Keyword(s):  
Vascular Permeability ◽  
Tyrosine Residues ◽  
Leukocyte Extravasation

Dissociation of VE-PTP from VE-cadherin is required for leukocyte extravasation and for VEGF-induced vascular permeability in vivo

2011 ◽  
Vol 195 (3) ◽  
pp. i4-i4
Author(s):  
Andre Broermann ◽  
Mark Winderlich ◽  
Helena Block ◽  
Maike Frye ◽  
Jan Rossaint ◽  
...  
Keyword(s):  
Vascular Permeability ◽  
Leukocyte Extravasation

scholarly journals Dissociation of VE-PTP from VE-cadherin is required for leukocyte extravasation and for VEGF-induced vascular permeability in vivo

2011 ◽  
Vol 208 (12) ◽  
pp. 2393-2401 ◽  
Author(s):  
Andre Broermann ◽  
Mark Winderlich ◽  
Helena Block ◽  
Maike Frye ◽  
Jan Rossaint ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Vascular Permeability ◽  
Fusion Proteins ◽  
Tyrosine Phosphatase ◽  
Cell Contact ◽  
Vascular Endothelial ◽  
Cell Contacts ◽  
Leukocyte Extravasation

We have recently shown that vascular endothelial protein tyrosine phosphatase (VE-PTP), an endothelial membrane protein, associates with VE-cadherin and is required for optimal VE-cadherin function and endothelial cell contact integrity. The dissociation of VE-PTP from VE-cadherin is triggered by vascular endothelial growth factor (VEGF) and by the binding of leukocytes to endothelial cells in vitro, suggesting that this dissociation is a prerequisite for the destabilization of endothelial cell contacts. Here, we show that VE-cadherin/VE-PTP dissociation also occurs in vivo in response to LPS stimulation of the lung or systemic VEGF stimulation. To show that this dissociation is indeed necessary in vivo for leukocyte extravasation and VEGF-induced vascular permeability, we generated knock-in mice expressing the fusion proteins VE-cadherin-FK 506 binding protein and VE-PTP-FRB* under the control of the endogenous VE-cadherin promoter, thus replacing endogenous VE-cadherin. The additional domains in both fusion proteins allow the heterodimeric complex to be stabilized by a chemical compound (rapalog). We found that intravenous application of the rapalog strongly inhibited VEGF-induced (skin) and LPS-induced (lung) vascular permeability and inhibited neutrophil extravasation in the IL-1β inflamed cremaster and the LPS-inflamed lung. We conclude that the dissociation of VE-PTP from VE-cadherin is indeed required in vivo for the opening of endothelial cell contacts during induction of vascular permeability and leukocyte extravasation.

scholarly journals ANTI-INFLAMMATORY ACTIVITY OF CURCUMIN AND CAPSAICIN AUGMENTED IN COMBINATION

2017 ◽  
Vol 9 (6) ◽  
pp. 145
Author(s):  
Thriveni Vasanth Kumar ◽  
Manjunatha H. ◽  
Rajesh Kp
Keyword(s):  
Acetic Acid ◽  
Protective Effect ◽  
Vascular Permeability ◽  
Diclofenac Sodium ◽  
Significant Inhibition ◽  
Inflammatory Activity ◽  
Anti Inflammatory ◽  
The Individual

Objective: Dietary curcumin and capsaicin are well known for their health beneficial potencies. The current study was done to assess the anti-inflammatory activity of curcumin, capsaicin and their combination by employing in vitro and in vivo models.Methods: We investigated the protective effect of curcumin, capsaicin and their combination using in vitro heat induced human red blood cell (HRBC) membrane stabilisation, in vivo 3% agar induced leukocyte mobilisation and acetic acid induced vascular permeability assay.Results: Curcumin, capsaicin and their combination exhibited concentration dependent protective effect against heat-induced HRBC membrane destabilisation, while combined curcumin and capsaicin restored 87.0±0.64 % membrane stability and it is found to be better than curcumin, capsaicin and diclofenac sodium (75.0±0.25. 72±0.9 and 80.0±0.31 %) protective effect. In agar suspension induced leukocyte mobilization assay, the combined curcumin and capsaicin had shown 39.5±1.58 % of inhibition compared to individual curcumin and capsaicin, which showed moderate inhibition of 16.0±3.14 and 21.6±2.17 % respectively. Besides, the combined curcumin and capsaicin had shown highly significant inhibition of acetic acid-induced vascular permeability in rats (62.0±3.14 %), whereas individual curcumin and capsaicin showed moderate inhibition of vascular permeability with 36.0±2.41 and 43.0±1.92 % respectively.Conclusion: This study demonstrates the significant anti-inflammatory property of combined curcumin and capsaicin at half of the individual concentration of curcumin and capsaicin.

Microcirculatory changes in sodium taurocholate-induced pancreatitis in rats

1991 ◽  
Vol 260 (2) ◽  
pp. G346-G351 ◽  
Author(s):  
K. Kusterer ◽  
M. Enghofer ◽  
S. Zendler ◽  
C. Blochle ◽  
K. H. Usadel
Keyword(s):  
Acute Pancreatitis ◽  
Blood Flow ◽  
Vascular Permeability ◽  
Sodium Taurocholate ◽  
Image Analyzer ◽  
In Vivo Microscopy ◽  
Microscopy Technique ◽  
Permeability Changes ◽  
Hemorrhagic Necrosis

Using an in vivo microscopy technique, we studied the microcirculatory changes in sodium taurocholate-induced pancreatitis in rats. With a computerized image analyzer system, blood flow, vascular permeability changes, and capillary densities were measured. Intraductal infusion of 0.4 ml saline had only minor effects on the microcirculation. Various concentrations and volumes of sodium taurocholate solutions were infused into the pancreatic duct. Sodium taurocholate (0.4 ml, 4%) led to increased vascular permeability preceding stasis within 232 +/- 47 s, followed by hemorrhagic necrosis in the head of the pancreas. In the corpus close to the tail of the pancreas capillary blood flow was maintained. In conclusion, this study shows that the microcirculation of the pancreas can be excellently investigated with in vivo microscopy. With this method, tremendous distribution disturbances of the microcirculation in the pancreas can be seen in the course of acute pancreatitis. Vascular permeability changes and stasis of the microcirculation represent the primary microcirculatory events in acute pancreatitis induced by sodium taurocholate in the areas where hemorrhagic necrosis occurs.

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