Expression profiling and pathway analysis of iron oxide nanoparticles toxicity on human lung alveolar epithelial cell line using microarray analysis

2020 ◽  
Vol 48 (4) ◽  
pp. 309-318
Author(s):  
Hasan TÜRKEZ ◽  
Mehmet Enes ARSLAN ◽  
Erdal SÖNMEZ ◽  
Abdulgani TATAR ◽  
Fatime GEYİKOĞLU ◽  
...  
Keyword(s):  
Iron Oxide ◽  
Epithelial Cell ◽  
Pathway Analysis ◽  
Expression Profiling ◽  
Human Lung ◽  
Alveolar Epithelial Cell ◽  
Epithelial Cell Line ◽  
Oxide Nanoparticles ◽  
Alveolar Epithelial ◽  
Nanoparticles Toxicity

Human Alveolar Epithelial Cell Responses to Core–Shell Superparamagnetic Iron Oxide Nanoparticles (SPIONs)

Langmuir ◽  
2015 ◽  
Vol 31 (13) ◽  
pp. 3829-3839 ◽  
Author(s):  
Doris Antoinette Mbeh ◽  
Laura Karina Mireles ◽  
Dimitri Stanicki ◽  
Lyes Tabet ◽  
Karim Maghni ◽  
...  
Keyword(s):  
Iron Oxide ◽  
Epithelial Cell ◽  
Iron Oxide Nanoparticles ◽  
Alveolar Epithelial Cell ◽  
Superparamagnetic Iron Oxide ◽  
Oxide Nanoparticles ◽  
Core Shell ◽  
Alveolar Epithelial ◽  
Cell Responses ◽  
Human Alveolar Epithelial Cell

Effect of Steroids on the Synthesis of Complement C3 in a Human Alveolar Epithelial Cell Line

1993 ◽  
Vol 19 (5) ◽  
pp. 603-616 ◽  
Author(s):  
Terence L. Zach ◽  
Vicki A. Herrman ◽  
Laura D. Hill ◽  
M. Patricia Leuschen
Keyword(s):  
Epithelial Cell ◽  
Cell Line ◽  
Alveolar Epithelial Cell ◽  
Complement C3 ◽  
Epithelial Cell Line ◽  
Alveolar Epithelial ◽  
Human Alveolar Epithelial Cell

A new rat type I-like alveolar epithelial cell line R3/1: bleomycin effects on caveolin expression

2004 ◽  
Vol 121 (6) ◽  
Author(s):  
Roland Koslowski ◽  
Kathrin Barth ◽  
Antje Augstein ◽  
Thomas Tschernig ◽  
Gerhard Bargsten ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Line ◽  
Alveolar Epithelial Cell ◽  
Epithelial Cell Line ◽  
Type I ◽  
Alveolar Epithelial

scholarly journals GED-0507 attenuates lung fibrosis by counteracting myofibroblast transdifferentiation in vivo and in vitro

PLoS ONE ◽  
2021 ◽  
Vol 16 (9) ◽  
pp. e0257281
Author(s):  
Silvia Speca ◽  
Caroline Dubuquoy ◽  
Christel Rousseaux ◽  
Philippe Chavatte ◽  
Pierre Desreumaux ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Pulmonary Fibrosis ◽  
Transforming Growth Factor ◽  
Alveolar Epithelial Cell ◽  
Lung Fibroblasts ◽  
Epithelial Cell Line ◽  
Mesenchymal Transition ◽  
Alveolar Epithelial ◽  
Ppar Γ

The development of more effective, better tolerated drug treatments for progressive pulmonary fibrosis (of which idiopathic pulmonary fibrosis is the most common and severe form) is a research priority. The peroxisome proliferator-activated receptor gamma (PPAR-γ) is a key regulator of inflammation and fibrosis and therefore represents a potential therapeutic target. However, the use of synthetic PPAR-γ agonists may be limited by their potentially severe adverse effects. In a mouse model of bleomycin (BLM)-induced pulmonary fibrosis, we have demonstrated that the non-racemic selective PPAR-γ modulator GED-0507 is able to reduce body weight loss, ameliorate clinical and histological features of pulmonary fibrosis, and increase survival rate without any safety concerns. Here, we focused on the biomolecular effects of GED-0507 on various inflammatory/fibrotic pathways. We demonstrated that preventive and therapeutic administration of GED-0507 reduced the BLM-induced mRNA expression of several markers of fibrosis, including transforming growth factor (TGF)-β, alpha-smooth muscle actin, collagen and fibronectin as well as epithelial-to-mesenchymal transition (EMT) and expression of mucin 5B. The beneficial effect of GED-0507 on pulmonary fibrosis was confirmed in vitro by its ability to control TGFβ-induced myofibroblast activation in the A549 human alveolar epithelial cell line, the MRC-5 lung fibroblast line, and primary human lung fibroblasts. Compared with the US Food and Drug Administration-approved antifibrotic drugs pirfenidone and nintedanib, GED-0507 displayed greater antifibrotic activity by controlling alveolar epithelial cell dysfunction, EMT, and extracellular matrix remodeling. In conclusion, GED-0507 demonstrated potent antifibrotic properties and might be a promising drug candidate for the treatment of pulmonary fibrosis.

Activation of L-type Ca2+ channels after purinoceptor stimulation by ATP in an alveolar epithelial cell (L2)

1995 ◽  
Vol 269 (6) ◽  
pp. L873-L883 ◽  
Author(s):  
P. Dietl ◽  
T. Haller ◽  
B. Wirleitner ◽  
H. Volkl ◽  
F. Friedrich ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Alveolar Epithelial Cell ◽  
Alveolar Epithelium ◽  
Bay K 8644 ◽  
Epithelial Cell Line ◽  
Apparent Dissociation Constant ◽  
Whole Cell ◽  
Fura 2 ◽  
Alveolar Epithelial ◽  
Ca2 Channels

In the alveolar epithelium, ATP increases the intracellular Ca2+ concentration ([Ca2+]i) and stimulates the secretion of surfactant. We investigated the effects of extracellular ATP on the membrane potential (Vm), the whole cell current, and [Ca2+]i in a cloned rat alveolar epithelial cell line (L2). In microelectrode experiments, ATP caused a sustained depolarization of Vm, resulting from the activation of cation and Cl- conductances, as revealed by ion replacements. The depolarizing phase of the Vm shift was superimposed by Ca(2+)-dependent depolarizing spikes. Spikes were also induced by depolarizing Vm with charybdotoxin or maitotoxin. Replacement of bath Ca2+ with Ba2+ or Sr2+ also evoked repetitive spikes. Ca2+ (Ba2+, Sr2+)-induced spikes were unaffected by pretreatment with ionomycin or thapsigargin. They were, however, completely abolished by (+)-isradipine (100 nM) and stimulated by BAY K 8644 (100 nM). Whole cell L-type Ca2+ (Ba2+, Sr2+) currents were similarly abolished by (+)-isradipine and enhanced by BAY K 8644. L-type Ca2+ channels were further confirmed by demonstrating high-affinity dihydropyridine receptors stereoselectively labeled by (+)-[3H]-isradipine, apparent dissociation constant < 1 nM. In fura 2 experiments, ATP evoked a transient elevation of [Ca2+]i in the absence of Ca2+ and a biphasic sustained elevation in the presence of Ca2+, indicating intracellular Ca2+ release and Ca2+ entry. The ATP-induced fura 2 signals were unaffected by (+)-isradipine. We conclude that in L2 cells, L-type Ca2+ channels are activated after purinoceptor stimulation by ATP. The overall [Ca2+]i response is, however, mediated by Ca2+ entry through and (+)-isradipine-insensitive mechanism and by intracellular Ca2+ release.

scholarly journals Neopterin and 7,8-dihydroneopterin induce apoptosis in the rat alveolar epithelial cell line L2

FEBS Letters ◽  
1996 ◽  
Vol 397 (2-3) ◽  
pp. 263-268 ◽  
Author(s):  
Wolfgang Schobersberger ◽  
Georg Hoffmann ◽  
Petra Hobisch-Hagen ◽  
Günther Böck ◽  
Harald Völkl ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Line ◽  
Alveolar Epithelial Cell ◽  
Epithelial Cell Line ◽  
Alveolar Epithelial
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