Evidence map›Paper›PMID 21932060›Full record

ArticleInflammation2012

Lentivirus-mediated ADAM17 RNA interference inhibited interleukin-8 expression via EGFR signaling in lung epithelial cells.

Yaqing Li, Jianping Yan, Wulin Xu, Hong Wang, Yingjie Xia

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 34% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
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

5 authors at 1 institution in 1 country.

Yaqing LiDepartment of Respiratory Medicine, Zhejiang Provincial People's Hospital, 158 Shangtang Road, Hangzhou, 310014, China. lidoctor03@126.com
Jianping Yan
Wulin Xu
Hong Wang
Yingjie Xia
Zhejiang Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interleukin (IL)-8 and neutrophil inflammation play a vital role in the pathogenesis of chronic inflammatory airway diseases. A disintegrin and metalloproteinase 17 (ADAM17) cleaves ectodomains of various transmembrane proteins and is an important regulator of almost every cellular event. The aim of this work was to investigate the roles of epidermal growth factor receptor (EGFR) signaling and ADAM17 in IL-8 expression induced by lipopolysaccharide (LPS) in A549 lung epithelial cells. In the present study, we found that transforming growth factor-α (TGF-α)-neutralizing Ab, EGFR-neutralizing Ab, and AG1478 significantly inhibited the phosphorylation of EGFR and IL-8 production induced by LPS. Lentivirus-mediated ADAM-17 RNA interference markedly inhibited ADAM-17 expression, the release of TGF-α, and the phosphorylation of EGFR and IL-8 expression. The results demonstrated that lentivirus-mediated RNA interference targeting ADAM17 suppressed IL-8 expression induced by LPS via inhibiting EGFR signaling, and ADAM17-EGFR signaling cascade mediated IL-8 production induced by LPS in lung epithelial cells.

Indexed as

ADAM17 ProteinADAM ProteinsAntibodies, NeutralizingCell LineEpithelial CellsErbB ReceptorsGenetic VectorsGene Transfer TechniquesHumansInflammationInterleukin-8LentivirusLipopolysaccharidesLungPhosphorylationQuinazolinesADAM17 ProteinADAM17 protein, humanADAM ProteinsAntibodies, NeutralizingEGFR protein, humanErbB ReceptorsInterleukin-8LipopolysaccharidesQuinazolinesRNA, Small InterferingRTKI cpdTransforming Growth Factor alphaTyrphostins

Identifiers

PMID21932060
OpenAlexW2096433206

What OpenQuestion holds

Textmetadata
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.