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17β-estradiol suppresses lipopolysaccharide-induced acute lung injury through PI3K/Akt/SGK1 mediated up-regulation of epithelial sodium channel (ENaC) in vivo and in vitro

Overview of attention for article published in Respiratory Research, December 2014
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  • Above-average Attention Score compared to outputs of the same age (51st percentile)
  • Average Attention Score compared to outputs of the same age and source

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4 X users
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1 Google+ user

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24 Mendeley
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Title
17β-estradiol suppresses lipopolysaccharide-induced acute lung injury through PI3K/Akt/SGK1 mediated up-regulation of epithelial sodium channel (ENaC) in vivo and in vitro
Published in
Respiratory Research, December 2014
DOI 10.1186/s12931-014-0159-1
Pubmed ID
Authors

Di Qi, Jing He, Daoxin Wang, Wang Deng, Yan Zhao, Yuan Ye, Longhua Feng

Abstract

Background17ß-estradiol can suppress acute lung injury (ALI) and regulate alveolar epithelial sodium channel (ENaC). However the relationship between these two functions remains unclear. This study is conducted to assess the role of ENaC and the PI3K/Akt/SGK1 signaling pathway in 17ß-estradiol therapy in attenuating LPS-induced ALI.MethodsALI was induced in C57BL/J male mice by intratracheal administration of lipopolysaccharide (LPS). Concurrent with LPS administration, 17ß-estradiol or sterile saline was administered to ALI model with or without the phosphoinositide 3-kinase (PI3K) inhibitor wortmannin. The lung histological changes, inflammatory mediators in bronchoalveolar lavage fluid (BALF), wet/dry weight ratio (W/D) and alveolar fluid clearance (AFC) were measured 4 hours after LPS challenge in vivo. For in vitro studies, LPS-challenged MLE-12 cells were pre-incubated with or without wortmannin for 30 minutes prior to 17ß-estradiol treatment. Expression of ENaC subunits was assessed by reverse transcriptase PCR, western blot, cell surface biotinylation, and immunohistochemistry. The levels of phosphorylated Akt and SGK1 in lung tissue and lung cell lines were investigated by western blot.Results17ß-estradiol suppressed LPS-mediated ALI in mice by diminishing inflammatory mediators and enhancing AFC. 17ß-estradiol promoted the expression and surface abundance of ¿-ENaC, and increased the levels of phosphorylated-Akt and phosphorylated-SGK1 following LPS challenge. This induction was abolished by the PI3K inhibitor wortmannin in vivo and in vitro.Conclusion17ß-estradiol attenuates LPS-induced ALI not only by repressing inflammation, but also by reducing pulmonary edema via elevation of ¿-ENaC expression and membrane abundance. These effects were mediated, at least partially, via activation of the PI3K/Akt/SGK1 signaling pathway.

X Demographics

X Demographics

The data shown below were collected from the profiles of 4 X users who shared this research output. Click here to find out more about how the information was compiled.
Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 24 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United States 1 4%
Unknown 23 96%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 8 33%
Student > Master 4 17%
Student > Bachelor 3 13%
Student > Postgraduate 2 8%
Professor > Associate Professor 2 8%
Other 2 8%
Unknown 3 13%
Readers by discipline Count As %
Medicine and Dentistry 6 25%
Biochemistry, Genetics and Molecular Biology 4 17%
Pharmacology, Toxicology and Pharmaceutical Science 3 13%
Agricultural and Biological Sciences 2 8%
Psychology 1 4%
Other 1 4%
Unknown 7 29%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 3. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 19 January 2015.
All research outputs
#8,534,528
of 25,373,627 outputs
Outputs from Respiratory Research
#1,153
of 3,062 outputs
Outputs of similar age
#110,193
of 359,100 outputs
Outputs of similar age from Respiratory Research
#25
of 47 outputs
Altmetric has tracked 25,373,627 research outputs across all sources so far. This one is in the 43rd percentile – i.e., 43% of other outputs scored the same or lower than it.
So far Altmetric has tracked 3,062 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 7.9. This one has gotten more attention than average, scoring higher than 56% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 359,100 tracked outputs that were published within six weeks on either side of this one in any source. This one has gotten more attention than average, scoring higher than 51% of its contemporaries.
We're also able to compare this research output to 47 others from the same source and published within six weeks on either side of this one. This one is in the 46th percentile – i.e., 46% of its contemporaries scored the same or lower than it.