Dataset Information

Lipoxin A₄ ameliorates lipopolysaccharide-induced lung injury through stimulating epithelial proliferation, reducing epithelial cell apoptosis and inhibits epithelial-mesenchymal transition.

ABSTRACT:

Background

Acute respiratory distress syndrome (ARDS) is characterized by alveolar epithelial disruption. Lipoxins (LXs), as so-called "braking signals" of inflammation, are the first mediators identified to have dual anti-inflammatory and inflammatory pro-resolving properties.

Methods

In vivo, lipoxinA₄ was administrated intraperitoneally with 1??g/per mouse after intra-tracheal LPS administration (10?mg/kg). Apoptosis, proliferation and epithelial-mesenchymal transition of AT II cells were measured by immunofluorescence. In vitro, primary human alveolar type II cells were used to model the effects of lipoxin A₄ upon proliferation, apoptosis and epithelial-mesenchymal transition.

Results

In vivo, lipoxin A₄ markedly promoted alveolar epithelial type II cells (AT II cells) proliferation, inhibited AT II cells apoptosis, reduced cleaved caspase-3 expression and epithelial-mesenchymal transition, with the outcome of attenuated LPS-induced lung injury. In vitro, lipoxin A₄ increased primary human alveolar epithelial type II cells (AT II cells) proliferation and reduced LPS induced AT II cells apoptosis. LipoxinA₄ also inhibited epithelial mesenchymal transition in response to TGF-?₁, which was lipoxin receptor dependent. In addition, Smad3 inhibitor (Sis3) and PI3K inhibitor (LY294002) treatment abolished the inhibitory effects of lipoxinA₄ on the epithelial mesenchymal transition of primary human AT II cells. Lipoxin A₄ significantly downregulated the expressions of p-AKT and p-Smad stimulated by TGF-?₁ in primary human AT II cells.

Conclusion

LipoxinA₄ attenuates lung injury via stimulating epithelial cell proliferation, reducing epithelial cell apoptosis and inhibits epithelial-mesenchymal transition.

SUBMITTER: Yang JX

PROVIDER: S-EPMC6704532 | biostudies-literature | 2019 Aug

REPOSITORIES: biostudies-literature

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Publications

Lipoxin A<sub>4</sub> ameliorates lipopolysaccharide-induced lung injury through stimulating epithelial proliferation, reducing epithelial cell apoptosis and inhibits epithelial-mesenchymal transition.

Yang Jing-Xiang JX Li Ming M Chen Xin-Ou XO Lian Qing-Quan QQ Wang Qian Q Gao Fang F Jin Sheng-Wei SW Zheng Sheng-Xing SX

Respiratory research 20190822 1

<h4>Background</h4>Acute respiratory distress syndrome (ARDS) is characterized by alveolar epithelial disruption. Lipoxins (LXs), as so-called "braking signals" of inflammation, are the first mediators identified to have dual anti-inflammatory and inflammatory pro-resolving properties.<h4>Methods</h4>In vivo, lipoxinA<sub>4</sub> was administrated intraperitoneally with 1 μg/per mouse after intra-tracheal LPS administration (10 mg/kg). Apoptosis, proliferation and epithelial-mesenchymal transiti ...[more]

PMID: 31438948

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Dataset Information

Lipoxin A₄ ameliorates lipopolysaccharide-induced lung injury through stimulating epithelial proliferation, reducing epithelial cell apoptosis and inhibits epithelial-mesenchymal transition.

Background

Methods

Results

Conclusion

Publications

Lipoxin A<sub>4</sub> ameliorates lipopolysaccharide-induced lung injury through stimulating epithelial proliferation, reducing epithelial cell apoptosis and inhibits epithelial-mesenchymal transition.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets

Dataset Information

Lipoxin A4 ameliorates lipopolysaccharide-induced lung injury through stimulating epithelial proliferation, reducing epithelial cell apoptosis and inhibits epithelial-mesenchymal transition.

Background

Methods

Results

Conclusion

Publications

Lipoxin A<sub>4</sub> ameliorates lipopolysaccharide-induced lung injury through stimulating epithelial proliferation, reducing epithelial cell apoptosis and inhibits epithelial-mesenchymal transition.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets

Lipoxin A₄ ameliorates lipopolysaccharide-induced lung injury through stimulating epithelial proliferation, reducing epithelial cell apoptosis and inhibits epithelial-mesenchymal transition.