Evidence map›Paper›PMID 33260152›Full record

ArticleAging2020

Cigarette smoke extract induces airway epithelial cell death via repressing PRMT6/AKT signaling.

Tiao Li, Kristen V Fanning, Toru Nyunoya, Yan Chen, Chunbin Zou

Open access · greenAbstract read
In one paragraph

Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.3field-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

22 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
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  11. m6A: a novel strategy for osteoporosis treatment.Frontiers in cell and developmental biology · 2025
    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 1 institution in 2 countries.

Tiao LiDepartment of Pulmonary and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha 410011, Hunan, China.
Kristen V FanningDivision of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.
Toru NyunoyaDivision of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.
Yan ChenDepartment of Pulmonary and Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha 410011, Hunan, China.
Chunbin ZouDivision of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.
University of Pittsburgh · US

Funding

Epigenetic Modulation in Septic ImmunosuppressionR01HL142997 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ZOU, CHUNBIN · 2019 to 2022
$1.8M
Role of TACC2 in smoking-induced COPDR01HL149719 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI NYUNOYA, TORU · 2020 to 2023
$1.6M
Epigenetic Regulation in Acute Lung InjuryR01HL125435 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ZOU, CHUNBIN · 2015 to 2018
$1.5M
Targeting F-box protein 048 in acute lung injuryI01CX000105 · VA · VETERANS HEALTH ADMINISTRATION · PI NYUNOYA, TORU · 2009 to 2022
–
CSRD VA I01 CX000105NHLBI NIH HHS R01 HL125435NHLBI NIH HHS R01 HL142997NHLBI NIH HHS R01 HL149719
6 · The paper itself

Abstract

Chronic obstructive pulmonary disease (COPD) is a severe public health threat world-wide. Cigarette smoke (CS)-induced airway epithelial cell death is a major pathway of pathogenesis in emphysema, a subtype of COPD. Protein arginine methyltransferase 6 (PRMT6) is a type I PRMT that catalyzes mono- and di-methylation on arginine residues within histone and non-histone proteins to modulate a variety of life processes, such as apoptosis. However, its role in CS-induced lung epithelial death has not been fully elucidated. Here we report that PRMT6 was decreased in mouse lung tissues from a cigarette smoke extract (CSE)-mediated experimental emphysematous model and in CSE treated or cigarette smoke exposed lung epithelial cells. Depletion of PRMT6 increased the protein levels of phosphatase PTEN and PI3K regulatory subunit p85 but decreased a downstream kinase PDK1, resulting in AKT dephosphorylation and thereafter, lung epithelial cell death. Knockout of PRMT6 inhibited epithelial survival and promoted CSE-mediated epithelial cell death, while ectopic expression of PRMT6 protein partially reversed epithelial cell death via PI3K/AKT-mediated cell survival signaling in CSE cellular models. These findings demonstrate that PRMT6 plays a crucial role in CS-induced bronchial epithelial cell death that may be a potential therapeutic target against the airway cell death in CS-induced COPD.

Indexed as

AnimalsCell DeathCell LineDisease Models, AnimalEpithelial CellsHumansLungMice, Inbred BALB CNuclear ProteinsPhosphatidylinositol 3-KinasePhosphorylationProtein-Arginine N-MethyltransferasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePulmonary EmphysemaSignal TransductionNuclear ProteinsPhosphatidylinositol 3-KinasePRMT6 protein, humanPRMT6 protein, mouseProtein-Arginine N-MethyltransferasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanPten protein, mouseSmokecell deathcigarette smokelung epitheliaPI3K/AKTPRMT6

Identifiers

PMID33260152
PMCPMC7762507
OpenAlexW3109301409

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.