scholarly journals Oxygen radicals mediate endothelial cell damage by complement-stimulated granulocytes. An in vitro model of immune vascular damage.

1978 ◽  
Vol 61 (5) ◽  
pp. 1161-1167 ◽  
Author(s):  
T Sacks ◽  
C F Moldow ◽  
P R Craddock ◽  
T K Bowers ◽  
H S Jacob
Keyword(s):  
Endothelial Cell ◽  
Oxygen Radicals ◽  
In Vitro Model ◽  
Cell Damage ◽  
Vascular Damage ◽  
Endothelial Cell Damage ◽  
Vitro Model

A two-insult in vitro model of PMN-mediated pulmonary endothelial damage: requirements for adherence and chemokine release

2002 ◽  
Vol 283 (6) ◽  
pp. C1592-C1603 ◽  
Author(s):  
Travis H. Wyman ◽  
A. Jason Bjornsen ◽  
David J. Elzi ◽  
C. Wayne Smith ◽  
Kelly M. England ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
In Vitro Model ◽  
Cell Damage ◽  
Endothelial Damage ◽  
Microvascular Endothelial Cells ◽  
Blood Storage ◽  
Endothelial Cell Damage ◽  
Vitro Model ◽  
Lps Activation

Lysophosphatidylcholines (lyso-PCs), generated during blood storage, are etiologic in a two-insult, sepsis-based model of transfusion-related acute lung injury (TRALI). Individually, endotoxin (LPS) and lyso-PCs prime but do not activate neutrophils (PMNs). We hypothesized that priming of PMNs alters their reactivity such that a second priming agent causes PMN activation and endothelial cell damage. PMNs were primed or not with LPS and then treated with lyso-PCs, and oxidase activation and elastase release were measured. For coculture experiments, activation of human pulmonary microvascular endothelial cells (HMVECs) was assessed by ICAM-1 expression and chemokine release. HMVECs were stimulated or not with LPS, PMNs were added, cells were incubated with lyso-PCs, and the number of viable HMVECs was counted. Lyso-PCs activated LPS-primed PMNs. HMVEC activation resulted in increased ICAM-1 and release of ENA-78, GROα, and IL-8. PMN-mediated HMVEC damage was dependent on LPS activation of HMVECs, chemokine release, PMN adhesion, and lyso-PC activation of the oxidase. In conclusion, sequential exposure of PMNs to priming agents activates the microbicidal arsenal, and PMN-mediated HMVEC damage was the result of two insults: HMVEC activation and PMN oxidase assembly.

An in vitro model for investigation of vitamin A effects on wound healing

2021 ◽  
pp. 1-6
Author(s):  
Hoda Keshmiri Neghab ◽  
Mohammad Hasan Soheilifar ◽  
Gholamreza Esmaeeli Djavid
Keyword(s):  
Wound Healing ◽  
Endothelial Cell ◽  
Vitamin A ◽  
In Vitro Model ◽  
Cellular Proliferation ◽  
Endothelial Cell Migration ◽  
Normal Fibroblast ◽  
Anti Inflammatory ◽  
Vitro Model

Abstract. Wound healing consists of a series of highly orderly overlapping processes characterized by hemostasis, inflammation, proliferation, and remodeling. Prolongation or interruption in each phase can lead to delayed wound healing or a non-healing chronic wound. Vitamin A is a crucial nutrient that is most beneficial for the health of the skin. The present study was undertaken to determine the effect of vitamin A on regeneration, angiogenesis, and inflammation characteristics in an in vitro model system during wound healing. For this purpose, mouse skin normal fibroblast (L929), human umbilical vein endothelial cell (HUVEC), and monocyte/macrophage-like cell line (RAW 264.7) were considered to evaluate proliferation, angiogenesis, and anti-inflammatory responses, respectively. Vitamin A (0.1–5 μM) increased cellular proliferation of L929 and HUVEC (p < 0.05). Similarly, it stimulated angiogenesis by promoting endothelial cell migration up to approximately 4 fold and interestingly tube formation up to 8.5 fold (p < 0.01). Furthermore, vitamin A treatment was shown to decrease the level of nitric oxide production in a dose-dependent effect (p < 0.05), exhibiting the anti-inflammatory property of vitamin A in accelerating wound healing. These results may reveal the therapeutic potential of vitamin A in diabetic wound healing by stimulating regeneration, angiogenesis, and anti-inflammation responses.

scholarly journals Estimation of the Genotoxicityof Hydrogen Peroxide and Antioxidant Actionof Halo Acid by the Method of Dna-Cometwith the Use of the Model of Transplantable Cell Cultures

2018 ◽  
pp. 40-43
Author(s):  
Olga Verle ◽  
Oleg Ostrovskiy ◽  
Valerian Verovskiy ◽  
Galina Dudchenko
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
In Vitro Model ◽  
Cell Damage ◽  
Protective Action ◽  
Genetic Material ◽  
Optimal Level ◽  
Pharmacological Agents ◽  
Vitro Model

In the framework of the study, the degree of defragmentation of DNA by the DNA-comet method is evaluated when exposed to the cell culture of hydrogen peroxide (H2O2), and an in vitro model is developed to evaluate the antioxidant activity of new pharmacological agents. The results of working with cell lines show that the percentage of damage to the genetic material of cells of intact samples does not greatly vary from the method of removing the cellular monolayer from the culture plastic. Concerning the effect of H2O2 as an inducer of oxidative stress on DNA cell damage, the optimal level of DNA defragmentation has been modeled for subsequent studies of the protective action of antioxidants.

Aortic endothelial cell damage induced by β-VLDL and macrophages in vitro

1990 ◽  
Vol 85 (2-3) ◽  
pp. 161-167 ◽  
Author(s):  
Nobuhiko Tanimura ◽  
Yujiro Asada ◽  
Tohru Hayashi ◽  
Atsushi Kisanuki ◽  
Akinobu Sumiyoshi
Keyword(s):  
Endothelial Cell ◽  
Cell Damage ◽  
Endothelial Cell Damage ◽  
Aortic Endothelial Cell ◽  
Aortic Endothelial

Development of immortalized human cerebromicrovascular endothelial cell line as an in vitro model of the human blood–brain barrier

1997 ◽  
Vol 11 (13) ◽  
pp. 1187-1197 ◽  
Author(s):  
Arumugam Muruganandam ◽  
Leonie Moorhouse Herx ◽  
Robert Monette ◽  
Jon P. Durkin ◽  
Danica B. Stanimirovic
Keyword(s):  
Endothelial Cell ◽  
Cell Line ◽  
Blood Brain Barrier ◽  
Human Blood ◽  
In Vitro Model ◽  
Brain Barrier ◽  
Endothelial Cell Line ◽  
Blood Brain ◽  
Vitro Model
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