Evidence map›Paper›PMID 32883320›Full record

ArticleRespiratory research2020

Oxidative stress mediates the apoptosis and epigenetic modification of the Bcl-2 promoter via DNMT1 in a cigarette smoke-induced emphysema model.

Huihui Zeng, Tiao Li, Xue He, Shan Cai, Hong Luo, Ping Chen, Yan Chen

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.0field-weighted citation impact, top 7% 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

26 citing papers in PubMed, 49 citations in OpenAlex.

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  16. Animal models and mechanisms of tobacco smoke-induced chronic obstructive pulmonary disease (COPD).Journal of toxicology and environmental health. Part B, Critical reviews · 2023
    Review
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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

7 authors at 1 institution in 1 country.

Huihui ZengDepartment of Pulmonary and Critical Care Medicine, the Second Xiangya Hospital, Central South University, No. 139 Renmin Road, Changsha, 410011, Hunan, China.
Tiao LiDepartment of Pulmonary and Critical Care Medicine, the Second Xiangya Hospital, Central South University, No. 139 Renmin Road, Changsha, 410011, Hunan, China.
Xue HeDepartment of Pulmonary and Critical Care Medicine, the Second Xiangya Hospital, Central South University, No. 139 Renmin Road, Changsha, 410011, Hunan, China.
Shan CaiDepartment of Pulmonary and Critical Care Medicine, the Second Xiangya Hospital, Central South University, No. 139 Renmin Road, Changsha, 410011, Hunan, China.
Hong LuoDepartment of Pulmonary and Critical Care Medicine, the Second Xiangya Hospital, Central South University, No. 139 Renmin Road, Changsha, 410011, Hunan, China.
Ping ChenDepartment of Pulmonary and Critical Care Medicine, the Second Xiangya Hospital, Central South University, No. 139 Renmin Road, Changsha, 410011, Hunan, China.
Yan ChenDepartment of Pulmonary and Critical Care Medicine, the Second Xiangya Hospital, Central South University, No. 139 Renmin Road, Changsha, 410011, Hunan, China. chenyan99727@csu.edu.cn.ORCID http://orcid.org/0000-0002-7713-6913
Central South University · CN

Funding

National Natural Science Foundation of China 81170036National Natural Science Foundation of China 81370143National Natural Science Foundation of China 81400032Natural Science Foundation of Hunan Province 09JJ3036Natural Science Foundation of Hunan Province 2019JJ50877
6 · The paper itself

Abstract

backgroundEmphysema is a crucial pathological characteristic of chronic obstructive pulmonary disease (COPD). Oxidative stress, apoptosis and epigenetic mechanisms contribute to the pathogenesis of emphysema. However, an attempt to accurately identify whether these mechanisms interact with each other and how they are triggered has never been conducted.

methodThe total reactive oxygen species (ROS) level, pulmonary apoptosis and B-cell lymphoma/leukemia-2 (Bcl-2) expression, an apoptosis regulator, were detected in samples from COPD patients. Bisulfite sequencing PCR (BSP) was conducted to observe the alterations in the methylation of the Bcl-2 promoter in specimens. The dysregulation of DNA methyltransferase enzyme 1 (DNMT1), a vital DNA methyltransferase enzyme, in the lungs of patients was confirmed through western blotting. To find out interactions between oxidative stress and DNA methylation in emphysema, mouse models were built with antioxidant treatment and DNMT1 silencing, and were examined with the pulmonary apoptosis, Bcl-2 and DNMT1 levels, and epigenetic alterations of Bcl-2.

resultsHigher ROS levels and pulmonary apoptosis were observed in COPD patients than in healthy controls. Downregulated Bcl-2 expression with increased promoter methylation and DNMT1 protein expression was found in COPD patients. Antioxidant treatment reduced the level of ROS, DNMT1 protein and emphysematous progression in the smoking models. Following DNMT1 blockade, smoking models showed improved lung function, pulmonary apoptosis, emphysematous progression, and increased Bcl-2 protein level with less promoter methylation than emphysema mice.

conclusionCigarette-induced oxidative stress mediates pulmonary apoptosis and hypermethylation of the Bcl-2 promoter in emphysema models through DNMT1.

Indexed as

AgedAnimalsApoptosisCigarette SmokingDNA (Cytosine-5-)-Methyltransferase 1EmphysemaEpigenesis, GeneticFemaleHumansInhalation ExposureLungMaleMiceMice, Inbred C57BLMiddle AgedOxidative StressDNA (Cytosine-5-)-Methyltransferase 1DNMT1 protein, humanProto-Oncogene Proteins c-bcl-2ApoptosisBcl-2DNMT1HypermethylationOxidative stress

Identifiers

PMID32883320
PMCPMC7469342
OpenAlexW3082006836

What OpenQuestion holds

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LicenceCC BY
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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.