Platelet-endothelial cell interactions in vitro following freeze-thaw injury or detergent treatment

1984 ◽  
Vol 237 (3) ◽  
Author(s):  
LynnR. Trusal ◽  
AlbertW. Guzman ◽  
DavidL. Moore
Keyword(s):  
Endothelial Cell ◽  
Cell Interactions ◽  
Freeze Thaw ◽  
Detergent Treatment

Preconditioning and adenosine in I/R-induced leukocyte-endothelial cell interactions

1998 ◽  
Vol 274 (4) ◽  
pp. H1230-H1238 ◽  
Author(s):  
Paul Kubes ◽  
Derrice Payne ◽  
Lena Ostrovsky
Keyword(s):  
Endothelial Cell ◽  
Leukocyte Adhesion ◽  
Vascular Dysfunction ◽  
Ischemia Reperfusion ◽  
Microvascular Dysfunction ◽  
Cell Interactions ◽  
Minor Role ◽  
Neutrophil Adhesion ◽  
Rolling Velocity

Recently, it was reported that preconditioning reduced leukocyte adhesion following ischemia-reperfusion (I/R). We further examined the effects of preconditioning and adenosine not only on neutrophil adhesion but also on neutrophil rolling and vascular dysfunction. Intravital microscopy revealed a decrease in neutrophil rolling velocity; a profound increase in neutrophil rolling, adhesion, and microvascular dysfunction; and a reduction in venular shear rates associated with 60 min ischemia and 60 min reperfusion in the feline mesentery. Preconditioning (5 min ischemia/10 min reperfusion) prevented subsequent I/R-induced slow neutrophil rolling, neutrophil adhesion, and microvascular dysfunction but did not affect the flux of rolling neutrophils. Adenosine deaminase A1and A2adenosine-receptor antagonists had only minor effects on the preconditioning responses. Pretreatment of vessels with exogenous adenosine reduced neutrophil adhesion and microvascular permeability and improved neutrophil rolling velocity and shear forces associated with I/R, but the flux of rolling neutrophils was not affected. Finally, in vitro experiments revealed that adenosine had absolutely no direct effect on neutrophil-endothelial cell interactions. In conclusion, our data suggest that adenosine plays only a minor role in preconditioned vessels and that adenosine per se may not directly affect neutrophil-endothelial cell interactions.

Ethanol enhances leukocyte-endothelial cell interactions in mesenteric venules

1990 ◽  
Vol 259 (4) ◽  
pp. G578-G583 ◽  
Author(s):  
P. R. Kvietys ◽  
M. A. Perry ◽  
T. S. Gaginella ◽  
D. N. Granger
Keyword(s):  
Endothelial Cell ◽  
Receptor Antagonist ◽  
Alcohol Intoxication ◽  
Leukotriene B4 ◽  
Cell Interactions ◽  
In Vivo Studies ◽  
Rolling Velocity ◽  
Neutrophil Adherence

In vivo studies have implicated neutrophils in the gastric mucosal injury produced by intraluminal administration of ethanol. However, in vitro studies indicate that ethanol inhibits various neutrophil functions such as adherence, chemotaxis, and degranulation. The aim of the present study was to assess whether ethanol, at clinically relevant concentrations, is proinflammatory in vivo. Ethanol (0.2, 1.0, 2.0, and 4.0%) was applied to the surface of the cat mesentery, and neutrophil adherence to venules (30 microns diam) and extravasation into the interstitium were quantitated using intravital microscopy. Hemodynamic parameters were also measured (venular diameter, red blood cell velocity, and leukocyte rolling velocity) or calculated (venular blood flow and wall shear stress). In this model ethanol produced a dose-dependent increase in neutrophil adherence and extravasation. The increase in leukocyte-endothelial cell interactions could not be attributed to alterations in hemodynamic factors. Pretreatment of animals with a monoclonal antibody (MoAb IB4) directed to the neutrophil CD11/CD18 adherence complex completely prevented the ethanol-induced neutrophil adherence and extravasation. Pretreatment with a leukotriene B4 (LTB4)-receptor antagonist (SC 41930) or a platelet-activating factor (PAF)-receptor antagonist (WEB 2170) did not alter the ethanol-induced neutrophil-endothelial interactions. We conclude that ethanol is proinflammatory at concentrations which may be achieved in the mucosal interstitium during acute alcohol intoxication. The ethanol-induced leukocyte adherence and extravasation is dependent on the expression of adhesive glycoproteins. The inflammatory mediators, PAF and LTB4, do not appear to play an important role in the leukocyte-endothelial cell interactions initiated by ethanol.

Characterization of microvascular cell cultures from normotensive and hypertensive rat brains: Pericyte—endothelial cell interactions in vitro

1987 ◽  
Vol 19 (2) ◽  
pp. 197-206 ◽  
Author(s):  
Ira M. Herman ◽  
Patricia M. Newcomb ◽  
John E. Coughlin ◽  
Stanley Jacobson
Keyword(s):  
Endothelial Cell ◽  
Cell Cultures ◽  
Cell Interactions ◽  
Hypertensive Rat

Analysis of Platelet, Tumor Cell and Endothelial Cell Interactions in Vivo and in Vitro

1987 ◽  
pp. 172-183 ◽  
Author(s):  
K. V. Honn ◽  
D. G. Menter ◽  
B. W. Steinert ◽  
J. D. Taylor ◽  
J. M. Onoda ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Tumor Cell ◽  
Cell Interactions

Effect of Placental Growth Factor on Trophoblast–Endothelial Cell Interactions In Vitro

2020 ◽  
Vol 27 (6) ◽  
pp. 1285-1292
Author(s):  
K. Chau ◽  
B. Xu ◽  
A. Hennessy ◽  
A. Makris
Keyword(s):  
Endothelial Cell ◽  
Growth Factor ◽  
Placental Growth Factor ◽  
Cell Interactions

Protein Kinase CK2 Regulates Leukocyte-Endothelial Cell Interactions during Ischemia and Reperfusion in Striated Skin Muscle

2016 ◽  
Vol 57 (1-2) ◽  
pp. 111-124 ◽  
Author(s):  
Emmanuel Ampofo ◽  
Daniela Widmaier ◽  
Mathias Montenarh ◽  
Michael D. Menger ◽  
Matthias W. Laschke
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Protein Kinase ◽  
Protein Kinase Ck2 ◽  
Tissue Injury ◽  
Cell Interactions ◽  
Ischemia And Reperfusion ◽  
Kinase Ck2

Background: Ischemia and reperfusion (I/R) causes tissue injury by inflammatory processes. This involves the upregulation of endothelial surface proteins by phospho-regulated signaling pathways, resulting in enhanced interactions of leukocytes with endothelial cells. Recently, we found that protein kinase CK2 is a crucial regulator of leukocyte-mediated inflammation. Therefore, in this study we investigated the involvement of CK2 in leukocyte-endothelial cell interactions during I/R injury. Methods: We first analyzed the inhibitory action of (E)-3-(2,3,4,5-tetrabromophenyl)acrylic acid (TBCA) and CX-4945 on CK2 kinase activity and the viability of human dermal microvascular endothelial cells (HDMEC). To mimic I/R conditions in vitro, HDMEC were exposed to hypoxia and reoxygenation and the expression of adhesion molecules was analyzed by flow cytometry. Moreover, we analyzed in vivo the effect of CK2 inhibition on leukocyte-endothelial cell interactions in the dorsal skinfold chamber model of I/R injury by means of repetitive intravital fluorescence microscopy and immunohistochemistry. Results: We found that TBCA and CX-4945 suppressed the activity of CK2 in HDMEC without affecting cell viability. This was associated with a significant downregulation of E-selectin and intercellular adhesion molecule (ICAM)-1 after in vitro hypoxia and reoxygenation. In vivo, CX-4945 treatment significantly decreased the numbers of adherent and transmigrated leukocytes in striated muscle tissue exposed to I/R. Conclusion: Our findings indicate that CK2 is involved in the regulation of leukocyte-endothelial cell interactions during I/R by mediating the expression of E-selectin and ICAM-1.

Spatio-Temporal Control of Hepatic Stellate Cell–Endothelial Cell Interactions for Reconstruction of Liver Sinusoids In Vitro

2012 ◽  
Vol 18 (9-10) ◽  
pp. 1045-1056 ◽  
Author(s):  
Junichi Kasuya ◽  
Ryo Sudo ◽  
Toshihiro Mitaka ◽  
Mariko Ikeda ◽  
Kazuo Tanishita
Keyword(s):  
Endothelial Cell ◽  
Hepatic Stellate Cell ◽  
Stellate Cell ◽  
Cell Interactions ◽  
Temporal Control ◽  
Liver Sinusoids ◽  
Spatio Temporal
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