Endothelial cell monolayers as a tool for studying microvascular pathophysiology

1997 ◽  
Vol 273 (6) ◽  
pp. G1189-G1199 ◽  
Author(s):  
Peter R. Kvietys ◽  
D. Neil Granger
Keyword(s):  
Endothelial Cell ◽  
In Vitro Model ◽  
Cultured Cells ◽  
Critical Role ◽  
In Vitro Models ◽  
Cell Monolayers ◽  
Biological Responses ◽  
Vitro Model

Endothelial cells contribute to a variety of biological responses that facilitate organ function. This critical role of the endothelial cell has resulted in the development of different in vitro models that utilize monolayers of cultured cells to simulate conditions that exist in the intact animal. This review focuses on endothelial cell monolayers as a model system for research on certain pathophysiological conditions affecting the gastrointestinal tract. The advantages and limitations of endothelial cell monolayers are addressed, along with evolving technologies and strategies that hold promise for extending the utility of this in vitro model for studies of gastrointestinal function and disease.

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 A Role of Intravenous Immunoglobulin in Human Parechovirus Type 3 Infection in an In Vitro Model

2016 ◽  
Vol 3 (suppl_1) ◽  
Author(s):  
Ryohei Izumita ◽  
Yuta Aizawa ◽  
Kanako Watanabe ◽  
Akihiko Saitoh
Keyword(s):  
Intravenous Immunoglobulin ◽  
In Vitro Model ◽  
Human Parechovirus ◽  
Vitro Model ◽  
Type 3

scholarly journals β-Naphthoflavone and Ethanol Reverse Mitochondrial Dysfunction in A Parkinsonian Model of Neurodegeneration

2020 ◽  
Vol 21 (11) ◽  
pp. 3955
Author(s):  
Jesus Fernandez-Abascal ◽  
Elda Chiaino ◽  
Maria Frosini ◽  
Gavin P. Davey ◽  
Massimo Valoti
Keyword(s):  
Complex I ◽  
In Vitro Model ◽  
Inhibitory Effects ◽  
Cyp Induction ◽  
Cyp Isoforms ◽  
Vitro Model ◽  
Complex I Activity ◽  
Cyp 2D6

The 1-methyl-4-phenylpyridinium (MPP+) is a parkinsonian-inducing toxin that promotes neurodegeneration of dopaminergic cells by directly targeting complex I of mitochondria. Recently, it was reported that some Cytochrome P450 (CYP) isoforms, such as CYP 2D6 or 2E1, may be involved in the development of this neurodegenerative disease. In order to study a possible role for CYP induction in neurorepair, we designed an in vitro model where undifferentiated neuroblastoma SH-SY5Y cells were treated with the CYP inducers β-naphthoflavone (βNF) and ethanol (EtOH) before and during exposure to the parkinsonian neurotoxin, MPP+. The toxic effect of MPP+ in cell viability was rescued with both βNF and EtOH treatments. We also report that this was due to a decrease in reactive oxygen species (ROS) production, restoration of mitochondrial fusion kinetics, and mitochondrial membrane potential. These treatments also protected complex I activity against the inhibitory effects caused by MPP+, suggesting a possible neuroprotective role for CYP inducers. These results bring new insights into the possible role of CYP isoenzymes in xenobiotic clearance and central nervous system homeostasis.

scholarly journals 2-Hydroxy-(4-methylseleno)butanoic Acid Is Used by Intestinal Caco-2 Cells as a Source of Selenium and Protects against Oxidative Stress

2019 ◽  
Vol 149 (12) ◽  
pp. 2191-2198
Author(s):  
Joan Campo-Sabariz ◽  
David Moral-Anter ◽  
M Teresa Brufau ◽  
Mickael Briens ◽  
Eric Pinloche ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
In Vitro Model ◽  
Thioredoxin Reductase ◽  
Protein Carbonyl ◽  
Butanoic Acid ◽  
H2o2 Treatment ◽  
Vitro Model ◽  
Gpx Activity

ABSTRACT Background Selenium (Se) participates in different functions in humans and other animals through its incorporation into selenoproteins as selenocysteine. Inadequate dietary Se is considered a risk factor for several chronic diseases associated with oxidative stress. Objective The role of 2-hydroxy-(4-methylseleno)butanoic acid (HMSeBA), an organic form of Se used in animal nutrition, in supporting selenoprotein synthesis and protecting against oxidative stress was investigated in an in vitro model of intestinal Caco-2 cells. Methods Glutathione peroxidase (GPX) and thioredoxin reductase (TXNRD) activities, selenoprotein P1 protein (SELENOP) and gene (SELENOP) expression, and GPX1 and GPX2 gene expression were studied in Se-deprived (FBS removal) and further HMSeBA-supplemented (0.1–625 μM, 72 h) cultures. The effect of HMSeBA supplementation (12.5 and 625 μM, 24 h) on oxidative stress induced by H2O2 (1 mM) was evaluated by the production of reactive oxygen species (ROS), 4-hydroxy-2-nonenal (4-HNE) adducts, and protein carbonyl residues compared with a sodium selenite control (SS, 5 μM). Results Se deprivation induced a reduction (P &lt; 0.05) in GPX activity (62%), GPX1 expression, and both SELENOP (33%) and SELENOP expression. In contrast, an increase (P &lt; 0.05) in GPX2 expression and no effect in TXNRD activity (P = 0.09) were observed. HMSeBA supplementation increased (P &lt; 0.05) GPX activity (12.5–625 μM, 1.68–1.82-fold) and SELENOP protein expression (250 and 625 μM, 1.87- and 2.04-fold). Moreover, HMSeBA supplementation increased (P &lt; 0.05) GPX1 (12.5 and 625 μM), GPX2 (625 μM), and SELENOP (12.5 and 625 μM) expression. HMSeBA (625 μM) was capable of decreasing (P &lt; 0.05) ROS (32%), 4-HNE adduct (49%), and protein carbonyl residue (75%) production after H2O2 treatment. Conclusion Caco-2 cells can use HMSeBA as an Se source for selenoprotein synthesis, resulting in protection against oxidative stress.

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