Evidence map›Paper›PMID 34243729›Full record

ArticleBMC pulmonary medicine2021

XIST promotes apoptosis and the inflammatory response in CSE-stimulated cells via the miR-200c-3p/EGR3 axis.

Panfeng Chen, Ping Jiang, Jianing Chen, Yang Yang, Xiumei Guo

Open access · goldAbstract read
In one paragraph

Article in BMC pulmonary medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
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  8. EGR3 reduces podocyte inflammatory damage in obesity related glomerulopathy by inhibiting the PRMT1Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024
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  18. Revealing lncRNA Biomarkers Related to Chronic Obstructive Pulmonary Disease Based on Bioinformatics.International journal of chronic obstructive pulmonary disease · 2022
    Article
  19. 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

5 authors at 4 institutions in 1 country.

Panfeng ChenDepartment of Respiratory and Critical Care Medicine, Tianjin First Central Hospital, No. 24 Fukang Road, Nankai District, Tianjin, 300192, China. chenpf1st@hotmail.com.
Ping JiangDepartment of Respiratory and Critical Care Medicine, Tianjin First Central Hospital, No. 24 Fukang Road, Nankai District, Tianjin, 300192, China.
Jianing ChenDepartment of Respiratory and Critical Care Medicine, Tianjin First Central Hospital, No. 24 Fukang Road, Nankai District, Tianjin, 300192, China.
Yang YangDepartment of Respiratory and Critical Care Medicine, Haihe Hospital, Tianjin, 300222, China.
Xiumei GuoDepartment of Orthopaedics, Baoding Second Central Hospital, Baoding, 072750, Hebei, China.
Tianjin First Center Hospital · CNBaoding People's Hospital · CNTianjin haihe hospital · CNTianjin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic obstructive pulmonary disease (COPD) is a disease that causes obstructed airways and abnormal inflammatory responses in the lungs. Early growth response 3 (EGR3) has been revealed to play a vital role in the regulation of the inflammatory response in certain diseases. We aimed to explore the role of EGR3 and its upstream mechanism in COPD. METHODS AND

resultIn the present study, 16HBE cells were treated with cigarette smoke extract (CSE) to mimic the inflammatory response in vitro. RT-qPCR revealed that the expression of EGR3 was upregulated in lungs from COPD patients. EGR3 expression in 16HBE cells was increased by CSE treatment. Moreover, flow cytometry analysis and western blot analysis showed that EGR3 downregulation inhibited 16HBE cell apoptosis. EGR3 silencing decreased the protein levels of IL-6, TNF-α, IL-1β and COX2 in CSE-stimulated 16HBE cells. In addition, EGR3 was targeted by microRNA-200c-3p (miR-200c-3p) in 16HBE cells. MiR-200c-3p expression was significantly decreased in lung tissues from COPD patients compared to that in healthy controls. Furthermore, miR-200c-3p bound to lncRNA X-inactive specific transcript (XIST) in 16HBE cells. Additionally, XIST expression was elevated in lung tissues from COPD patients. Rescue assays indicated that EGR3 overexpression counteracted the effects of XIST downregulation on apoptosis and inflammation in CSE-stimulated 16HBE cells.

conclusionThe XIST/miR-200c-3p/EGR3 axis facilitated apoptosis and inflammation in CSE-stimulated 16HBE cells. These findings may provide novel insight for treating COPD by alleviating lung inflammation.

Indexed as

ApoptosisAdultAgedCell ProliferationCigarette SmokingCytokinesEarly Growth Response Protein 3FemaleHumansInflammationMaleMicroRNAsMiddle AgedPulmonary Disease, Chronic ObstructiveRNA, Long NoncodingCytokinesEarly Growth Response Protein 3EGR3 protein, humanMicroRNAsMIRN200 microRNA, humanRNA, Long NoncodingXIST non-coding RNAChronic obstructive pulmonary diseaseEGR3miR-200c-3pXIST

Identifiers

PMID34243729
PMCPMC8268373
OpenAlexW3178832504

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LicenceCC BY
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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.