Evidence map›Paper›PMID 24995336›Full record

ArticleBioMed research international2014

p120 modulates LPS-induced NF-κB activation partially through RhoA in bronchial epithelial cells.

Lingzhi Qin, Shenghui Qin, Yanli Zhang, Chao Zhang, Heng Ma, Naping Li, Liwei Liu, Xi Wang, Renliang Wu

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

15 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
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  3. Functions of p120-catenin in physiology and diseases.Frontiers in molecular biosciences · 2024
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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

9 authors at 1 institution in 1 country.

Lingzhi QinKey Laboratory of Pulmonary Disease of Ministry of Health of China, Institute of Pathology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.ORCID 0000-0003-4958-5241
Shenghui QinKey Laboratory of Pulmonary Disease of Ministry of Health of China, Institute of Pathology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.
Yanli ZhangKey Laboratory of Pulmonary Disease of Ministry of Health of China, Institute of Pathology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.
Chao ZhangKey Laboratory of Pulmonary Disease of Ministry of Health of China, Institute of Pathology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.ORCID 0000-0002-1458-8170
Heng MaKey Laboratory of Pulmonary Disease of Ministry of Health of China, Institute of Pathology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.ORCID 0000-0002-1141-7405
Naping LiKey Laboratory of Pulmonary Disease of Ministry of Health of China, Institute of Pathology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.ORCID 0000-0001-5398-7986
Liwei LiuKey Laboratory of Pulmonary Disease of Ministry of Health of China, Institute of Pathology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.
Xi WangKey Laboratory of Pulmonary Disease of Ministry of Health of China, Institute of Pathology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.ORCID 0000-0003-4378-3431
Renliang WuKey Laboratory of Pulmonary Disease of Ministry of Health of China, Institute of Pathology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.
Tongji Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

p120-Catenin (p120) is an adherens junction protein recognized to regulate cell-cell adhesion. Emerging evidence indicates that p120 may also play an important role in inflammatory responses, and the regulatory mechanisms are still unknown. In the present study, we showed that p120 was associated with airway inflammation. p120 downregulation induced nuclear factor-κB (NF-κB) activation, accompanied with I κ B α degradation, p65 nuclear translocation, and increased expression of interleukin-8 (IL-8) in lipopolysaccharide (LPS)- treated C57BL mice and human bronchial epithelial cells (BECs). Moreover, we first found that p120 directly coprecipitated with RhoA in BECs. After LPS stimulation, although total RhoA and p120-bound RhoA were unchanged, RhoA activity was increased. Y27632, a ROCK inhibitor, could partially inhibit nuclear translocation of p65. Overexpression of p120 inactivated RhoA and NF-κB in BECs, whereas p120 loss significantly increased RhoA activity, p65 nuclear translocation, and IL-8 expression. Taken together, our study supports the regulatory role of p120 in airway inflammation and reveals that p120 may modulate NF-κB signaling partially through RhoA.

Indexed as

AnimalsBronchiCateninsDelta CateninEpithelial CellsGene Expression RegulationHumansInflammationInterleukin-8LipopolysaccharidesNF-kappa BrhoA GTP-Binding ProteinSignal TransductionCateninsCTNND1 protein, humanDelta CateninInterleukin-8LipopolysaccharidesNF-kappa BrhoA GTP-Binding ProteinRHOA protein, human

Identifiers

PMID24995336
PMCPMC4065672
OpenAlexW2056712349

What OpenQuestion holds

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Registered trials

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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.