Evidence map›Paper›PMID 25551628›Full record

ArticleRespiratory research2014

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.

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

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.7field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

38 citing papers in PubMed, 72 citations in OpenAlex.

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  16. Possible protective role of 17β-estradiol against COVID-19.Journal of allergy and infectious diseases · 2020
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Di Qi
Jing He
Daoxin Wang
Wang Deng
Yan Zhao
Yuan Ye
Longhua Feng
Dalian Medical University · CNChongqing Medical University · CNSecond Affiliated Hospital of Chongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background17β-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 17β-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, 17β-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 17β-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.

results17β-estradiol suppressed LPS-mediated ALI in mice by diminishing inflammatory mediators and enhancing AFC. 17β-estradiol promoted the expression and surface abundance of α-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.

conclusion17β-estradiol attenuates LPS-induced ALI not only by repressing inflammation, but also by reducing pulmonary edema via elevation of α-ENaC expression and membrane abundance. These effects were mediated, at least partially, via activation of the PI3K/Akt/SGK1 signaling pathway.

Indexed as

EndotoxinsAcute Lung InjuryAnimalsBronchoalveolar Lavage FluidCell LineCytoprotectionDisease Models, AnimalEnzyme ActivationEpithelial Sodium ChannelsEstradiolImmediate-Early ProteinsInflammation MediatorsLungMaleMice, Inbred BALB CMice, Inbred C57BLendotoxin, Escherichia coliEndotoxinsEpithelial Sodium ChannelsEstradiolImmediate-Early ProteinsInflammation MediatorsPhosphatidylinositol 3-KinasePhosphoinositide-3 Kinase InhibitorsProtein Kinase InhibitorsProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktScnn1a protein, mouseSerum-Glucocorticoid Regulated Kinases

Identifiers

PMID25551628
PMCPMC4299800
OpenAlexW2119918621

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.