Evidence map›Paper›PMID 26617781›Full record

ArticleInternational journal of clinical and experimental pathology2015

USP17-mediated deubiquitination and stabilization of HDAC2 in cigarette smoke extract-induced inflammation.

Huihui Song, Lianqin Tao, Chen Chen, Lina Pan, Jimin Hao, Yingmeng Ni, Dan Li, Bin Li, Guochao Shi

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.5field-weighted citation impact, top 33% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

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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 2 institutions in 1 country.

Huihui SongDepartment of Pulmonary Medicine, Rui Jin Hospital, School of Medicine, Shanghai Jiao Tong University Shanghai 200025, P. R China.
Lianqin TaoDepartment of Pulmonary Medicine, Rui Jin Hospital, School of Medicine, Shanghai Jiao Tong University Shanghai 200025, P. R China.
Chen ChenKey Laboratory of Molecular Virology and Immunology, Unit of Molecular Immunology, Institute Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences (CAS) Shanghai 200031, P. R China.
Lina PanDepartment of Pulmonary Medicine, Rui Jin Hospital, School of Medicine, Shanghai Jiao Tong University Shanghai 200025, P. R China.
Jimin HaoDepartment of Pulmonary Medicine, Rui Jin Hospital, School of Medicine, Shanghai Jiao Tong University Shanghai 200025, P. R China.
Yingmeng NiDepartment of Pulmonary Medicine, Rui Jin Hospital, School of Medicine, Shanghai Jiao Tong University Shanghai 200025, P. R China.
Dan LiKey Laboratory of Molecular Virology and Immunology, Unit of Molecular Immunology, Institute Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences (CAS) Shanghai 200031, P. R China.
Bin LiKey Laboratory of Molecular Virology and Immunology, Unit of Molecular Immunology, Institute Pasteur of Shanghai, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences (CAS) Shanghai 200031, P. R China.
Guochao ShiDepartment of Pulmonary Medicine, Rui Jin Hospital, School of Medicine, Shanghai Jiao Tong University Shanghai 200025, P. R China.
Ruijin Hospital · CNInstitut Pasteur of Shanghai · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone deacetylase HDAC2 regulates genes transcription via removing the acetyl group from histones. Glucocorticoids, the most potent anti-inflammatory treatment available for inflammatory diseases, inhibit the expression of inflammatory genes by recruiting HDAC2 to activated genes. In the lungs of patients who smoke and have chronic obstructive pulmonary disease (COPD) or asthma, glucocorticoids are not effective enough to suppress airway inflammation, which is so called "glucocorticoid resistance", due to decreased HDAC2 level caused by cigarette smoke. We report that the ubiquitin-specific protease USP17 interacts with HDAC2. USP17 deubiquitinates and stabilizes the protein level of HDAC2. In cigarette smoke extract-exposed airway epithelial cells and macrophages, HDAC2 is excessively ubiquitinated and degraded in the proteasome attributed to low expression of USP17. Furthermore, over-expression of USP17 blocks the destruction of HDAC2 induced by cigarette smoke extract. These results provide a new insight into the mechanisms of glucocorticoid resistance in airway inflammatory disease. Small molecules which can specifically induce the expression of USP17 might be useful in reversing glucocorticoid resistance.

Indexed as

Protein Processing, Post-TranslationalCell Line, TumorEndopeptidasesEnzyme StabilityEpithelial CellsHEK293 CellsHistone Deacetylase 2HumansLungMacrophagesPneumoniaProteasome Endopeptidase ComplexProteolysisSmokeSmokingTime FactorsEndopeptidasesHDAC2 protein, humanHistone Deacetylase 2Proteasome Endopeptidase ComplexSmokeUSP17L2 protein, humancigarette smoke extractdeubiquitinationglucocorticoid resistanceHDAC2USP17

Identifiers

PMID26617781
PMCPMC4637596
OpenAlexW2413708986

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.