Evidence map›Paper›PMID 22891281›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

Shp2 plays an important role in acute cigarette smoke-mediated lung inflammation.

Fen-Fen Li, Jian Shen, Hui-Juan Shen, Xue Zhang, Rui Cao, Yun Zhang, Qiu Qui, Xi-Xi Lin, Yi-Cheng Xie, Lin-Hui Zhang and 10 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 17% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

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  16. Protein tyrosine phosphatase 11 acts through RhoA/ROCK to regulate eosinophil accumulation in the allergic airway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
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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

20 authors at 3 institutions in 1 country.

Fen-Fen LiDepartment of Pathology and Pathophysiology, Program in Molecular Cell Biology, Zhejiang University School of Medicine, Hangzhou, China 310058.
Jian Shen
Hui-Juan Shen
Xue Zhang
Rui Cao
Yun Zhang
Qiu Qui
Xi-Xi Lin
Yi-Cheng Xie
Lin-Hui Zhang
Yong-Liang Jia
Xin-Wei Dong
Jun-Xia Jiang
Meng-Jing Bao
Shanshan Zhang
Wen-Jiang Ma
Xi-Mei Wu
Huahao Shen
Qiang-Min Xie
Yuehai Ke
Zhejiang University · CNZheJiang Institute For Food and Drug Control · CNNational Medical Products Administration · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cigarette smoke (CS), the major cause of chronic obstructive pulmonary disease, contains a variety of oxidative components that were implicated in the regulation of Src homology domain 2-containing protein tyrosine phosphatase 2 (Shp2) activity. However, the contribution of Shp2 enzyme to chronic obstructive pulmonary disease pathogenesis remains unclear. We investigated the role of Shp2 enzyme in blockading CS-induced pulmonary inflammation. Shp2 levels were assessed in vivo and in vitro. Mice (C57BL/6) or pulmonary epithelial cells (NCI-H292) were exposed to CS or cigarette smoke extract (CSE) to induce acute injury and inflammation. Lungs of smoking mice showed increased levels of Shp2, compared with those of controls. Treatment of lung epithelial cells with CSE showed elevated levels of Shp2 associated with the increased release of IL-8. Selective inhibition or knockdown of Shp2 resulted in decreased IL-8 release in response to CSE treatment in pulmonary epithelial cells. In comparison with CS-exposed wild-type mice, selective inhibition or conditional knockout of Shp2 in lung epithelia reduced IL-8 release and pulmonary inflammation in CS-exposed mice. In vitro biochemical data correlate CSE-mediated IL-8 release with Shp2-regulated epidermal growth factor receptor/Grb-2-associated binders/MAPK signaling. Our data suggest an important role for Shp2 in the pathological alteration associated with CS-mediated inflammation. Shp2 may be a potential target for therapeutic intervention for inflammation in CS-induced pulmonary diseases.

Indexed as

Acute DiseaseAnimalsCell LineDisease Models, AnimalInflammationInterleukin-8MiceMice, Inbred C57BLMice, KnockoutMice, TransgenicPneumoniaProtein Tyrosine Phosphatase, Non-Receptor Type 11Pulmonary AlveoliRespiratory MucosaSmokingTobacco ProductsInterleukin-8Protein Tyrosine Phosphatase, Non-Receptor Type 11Ptpn11 protein, mouse

Identifiers

PMID22891281
PMCPMC3496208
OpenAlexW2101374510

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.