Evidence map›Paper›PMID 25897215›Full record

ArticleInternational journal of chronic obstructive pulmonary disease2015

Rosiglitazone attenuates the metalloprotease/anti-metalloprotease imbalance in emphysema induced by cigarette smoke: involvement of extracellular signal-regulated kinase and NFκB signaling.

Gang Hou, Yan Yin, Dan Han, Qiu-Yue Wang, Jian Kang

Open access · goldAbstract read
In one paragraph

Article in International journal of chronic obstructive pulmonary disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

19 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
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  3. The TIMP protein family: diverse roles in pathophysiology.American journal of physiology. Cell physiology · 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

5 authors at 1 institution in 1 country.

Gang HouDepartment of Respiratory Medicine, the First Hospital of China Medical University, Shenyang, People's Republic of China.
Yan YinDepartment of Respiratory Medicine, the First Hospital of China Medical University, Shenyang, People's Republic of China.
Dan HanDepartment of Respiratory Medicine, the First Hospital of China Medical University, Shenyang, People's Republic of China.
Qiu-Yue WangDepartment of Respiratory Medicine, the First Hospital of China Medical University, Shenyang, People's Republic of China.
Jian KangDepartment of Respiratory Medicine, the First Hospital of China Medical University, Shenyang, People's Republic of China.
First Hospital of China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveWe investigated how rosiglitazone attenuated cigarette smoke (CS)-induced emphysema in a rat model. In particular, we focused on its possible effects on the imbalance between metalloprotease (MMP) and anti-MMP activity, mitogen-activated protein kinase (MAPK) phosphorylation, and nuclear factor kappa-light-chain-enhancer of activated B cell (NFκB) signaling pathway over-activation.

methodsA total of 36 Wistar rats were divided into three groups (n=12 each): animals were exposed to CS for 12 weeks in the absence (the CS group) or presence of 30 mg/kg rosiglitazone (the rosiglitazone-CS [RCS] group); a control group was treated with the rosiglitazone vehicle only, without any CS exposure. Histopathology of lung tissue in all groups was evaluated to grade severity of the disease. Expression levels of peroxisome proliferator-activated receptor γ (PPARγ), MMP2, and MMP9 in lung tissue were determined and compared using Western blotting and immunohistochemistry. Activation of MAPKs, NFκB, and the nuclear factor of kappa light polypeptide gene enhancer in B-cell inhibitor, alpha (IκBα) phosphorylation in lung tissue was examined by Western blotting.

resultsEmphysema-related pathology, based on inter-alveolar wall distance and alveolar density, was less severe in the RCS group than in the CS group. Compared with the CS group, levels of PPARγ were higher in the RCS group, and levels of MMP2 and MMP9 proteins were lower in the RCS rats. Levels of activated MAPKs and NFκB were also lower, while the IκBα phosphorylation was increased in the lung tissue of RCS rats.

conclusionOur findings suggest that oral administration of rosiglitazone attenuates the metalloprotease activity induced by CS, and the underlying mechanism might involve the activation of signaling pathways dependent on MAPKs or NFκB. Our results further suggest that PPARγ contributes to the pathogenesis of emphysema as well as airway inflammation induced by CS.

Indexed as

Administration, OralAnimalsApoptosisCytoprotectionDisease Models, AnimalEnzyme ActivationExtracellular Signal-Regulated MAP KinasesI-kappa B ProteinsInhalation ExposureLungMaleMatrix Metalloproteinase 2Matrix Metalloproteinase 9NF-kappa BNF-KappaB Inhibitor alphaPhosphorylationExtracellular Signal-Regulated MAP KinasesI-kappa B ProteinsMatrix Metalloproteinase 2Matrix Metalloproteinase 9Mmp2 protein, ratMmp9 protein, ratNF-kappa BNF-KappaB Inhibitor alphaNfkbia protein, ratPPAR gammaRosiglitazoneSmokeThiazolidinedionesTobacco Smoke Pollutionchronic obstructive pulmonary diseaseemphysemamatrix metalloprotease2matrix metalloprotease9NFκBPPAR

Identifiers

PMID25897215
PMCPMC4396520
OpenAlexW1979807853

What OpenQuestion holds

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LicenceCC BY-NC
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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.