scholarly journals Botulinum toxin type A induces protective autophagy in human dermal microvascular endothelial cells exposed to an in�vitro model of ischemia/reperfusion injury

2018 ◽  
Author(s):  
Yanyu Shi ◽  
Huang Lin ◽  
Jiankun Cao ◽  
Chao Cui
Keyword(s):  
Endothelial Cells ◽  
Botulinum Toxin ◽  
In Vitro Model ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Botulinum Toxin Type A ◽  
Botulinum Toxin Type ◽  
Microvascular Endothelial Cells ◽  
Vitro Model

Novel In Vitro Model For Studying Hepatic Ischemia-Reperfusion Injury Using Liver Cubes

2011 ◽  
Vol 165 (2) ◽  
pp. 281-282
Author(s):  
B.J. DuBray ◽  
K.D. Conzen ◽  
G.A. Upadhya ◽  
P. Balachandran ◽  
J. Jia ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
In Vitro Model ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Hepatic Ischemia ◽  
Vitro Model ◽  
Hepatic Ischemia Reperfusion

scholarly journals Donor antibodies to HNA-3a implicated in TRALI reactions prime neutrophils and cause PMN-mediated damage to human pulmonary microvascular endothelial cells in a two-event in vitro model

Blood ◽  
2006 ◽  
Vol 109 (4) ◽  
pp. 1752-1755 ◽  
Author(s):  
Christopher C. Silliman ◽  
Brian R. Curtis ◽  
Patricia M. Kopko ◽  
Samina Y. Khan ◽  
Marguerite R. Kelher ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
In Vitro Model ◽  
Microvascular Endothelial Cells ◽  
Pulmonary Microvascular Endothelial Cells ◽  
Biologic Response ◽  
Event Model ◽  
Microvascular Endothelial ◽  
Vitro Model ◽  
Related Mortality

Abstract Transfusion-related acute lung injury (TRALI) is the leading cause of transfusion-related mortality. Antibodies to HNA-3a are commonly implicated in TRALI. We hypothesized that HNA-3a antibodies prime neutrophils (PMNs) and cause PMN-mediated cytotoxicity through a two-event pathogenesis. Isolated HNA-3a+ or HNA-3a− PMNs were incubated with plasma containing HNA-3a antibodies implicated in TRALI, and their ability to prime the oxidase was measured. Human pulmonary microvascular endothelial cells (HMVECs) were activated with endotoxin or buffer, HNA-3a+ or HNA-3a− PMNs were added, and the coculture was incubated with plasma ± antibodies to HNA-3a. PMN-mediated damage was measured by counting viable HMVECs/mm2. Plasma containing HNA-3a antibodies primed the fMLP-activated respiratory burst of HNA-3a+, but not HNA-3a−, PMNs and elicited PMN-mediated damage of LPS-activated HMVECs when HNA-3a+, but not HNA-3a−, PMNs were used. Thus, antibodies to HNA-3a primed PMNs and caused PMN-mediated HMVEC cytotoxicity in a two-event model identical to biologic response modifiers implicated in TRALI.

An in vitro model of ischemia/reperfusion-induced microvascular injury

1990 ◽  
Vol 259 (1) ◽  
pp. G134-G139 ◽  
Author(s):  
W. Inauen ◽  
D. N. Granger ◽  
C. J. Meininger ◽  
M. E. Schelling ◽  
H. J. Granger ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
In Vitro Model ◽  
Cell Injury ◽  
Ischemia Reperfusion ◽  
In Vivo Studies ◽  
Cell Detachment ◽  
51Cr Release ◽  
Vitro Model

The major objective of this study was to develop an in vitro model of ischemia/reperfusion (I/R)-induced microvascular injury. Cultured venular endothelial cells were grown to confluency, labeled with 51Cr, and exposed to different durations of anoxia (0.5, 1, 2, 3, and 4 h). 51Cr release and cell detachment (indexes of cell injury) were determined at different times after reoxygenation (1, 2, 4, 6, 8, and 18 h). Because in vivo studies have implicated neutrophils in I/R injury, in some experiments human neutrophils were added to the endothelial cells upon reoxygenation. Periods of anoxia greater than or equal to 2 h resulted in 70-80% 51Cr release and 80-95% cell detachment upon reoxygenation. Under these conditions (near maximal injury), the addition of neutrophils produced negligible effects. Periods of anoxia less than or equal to 1 h resulted in 30-40% 51Cr release and 50-60% cell detachment. Under these conditions (moderate cell injury), addition of neutrophils enhanced endothelial cell injury. Using a 30-min period of anoxia, we also assessed the effects of superoxide dismutase (SOD; 300 U/ml) and allopurinol (20 microM) on anoxia/reoxygenation (A/R)-induced injury in the presence or absence of neutrophils. In the absence of neutrophils, SOD or allopurinol did not protect against A/R-induced injury. However, in the presence of neutrophils, both SOD and allopurinol attenuated the increases in 51Cr release. The results derived using this in vitro model of I/R injury are largely consistent with published in vivo studies. Thus this in vitro model may provide further insights regarding the mechanisms involved in I/R injury.

A New in Vitro Model for Agonist-Induced Communication between Microvascular Endothelial Cells

2000 ◽  
Vol 60 (3) ◽  
pp. 222-231 ◽  
Author(s):  
Yves Ouellette ◽  
Darcy Lidington ◽  
Christian G. Naus ◽  
Karel Tyml
Keyword(s):  
Endothelial Cells ◽  
In Vitro Model ◽  
Microvascular Endothelial Cells ◽  
Microvascular Endothelial ◽  
Vitro Model
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