Evidence map›Paper›PMID 27793800›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2016

Gene expression profiling of epigenetic chromatin modification enzymes and histone marks by cigarette smoke: implications for COPD and lung cancer.

Isaac K Sundar, Irfan Rahman

Abstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.0field-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

39 citing papers in PubMed, 61 citations in OpenAlex.

  1. Air pollution-induced airway epithelial barrier dysfunction in COPD: a narrative review of mechanisms and therapeutic implications.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  2. Article
  3. Review
  4. Molecular underpinnings of induced degenerative heterogeneity in the retinal pigment epithelium.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  5. Article
  6. Review
  7. Article
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  10. A prognosis prediction chromatin regulator signature for patients with severe asthma.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2023
    Article
  11. Variations inGenes · 2023
    Article
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  13. 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

2 authors at 1 institution in 1 country.

Isaac K SundarDepartment of Environmental Medicine, University of Rochester Medical Center, Rochester, New York.
Irfan RahmanDepartment of Environmental Medicine, University of Rochester Medical Center, Rochester, New York irfan_rahman@urmc.rochester.edu.
University of Rochester Medical Center · US

Funding

VISUAL INDICES OF NEUROTOXICITYP30ES001247 · NIEHS · UNIVERSITY OF ROCHESTER · PI Sally W Thurston · 1985 to 2026
$42.8M
MECHANISMS OF CIGARETTE SMOKE-INDUCED LUNG CELLULAR SENESCENCER01HL085613 · NHLBI · UNIVERSITY OF ROCHESTER · PI RAHMAN, IRFAN · 2007 to 2017
$4.0M
NHLBI NIH HHS R01 HL085613NIEHS NIH HHS P30 ES001247
6 · The paper itself

Abstract

Chromatin-modifying enzymes mediate DNA methylation and histone modifications on recruitment to specific target gene loci in response to various stimuli. The key enzymes that regulate chromatin accessibility for maintenance of modifications in DNA and histones, and for modulation of gene expression patterns in response to cigarette smoke (CS), are not known. We hypothesize that CS exposure alters the gene expression patterns of chromatin-modifying enzymes, which then affects multiple downstream pathways involved in the response to CS. We have, therefore, analyzed chromatin-modifying enzyme profiles and validated by quantitative real-time PCR (qPCR). We also performed immunoblot analysis of targeted histone marks in C57BL/6J mice exposed to acute and subchronic CS, and of lungs from nonsmokers, smokers, and patients with chronic obstructive pulmonary disease (COPD). We found a significant increase in expression of several chromatin modification enzymes, including DNA methyltransferases, histone acetyltransferases, histone methyltransferases, and SET domain proteins, histone kinases, and ubiquitinases. Our qPCR validation data revealed a significant downregulation of Dnmt1, Dnmt3a, Dnmt3b, Hdac2, Hdac4, Hat1, Prmt1, and Aurkb We identified targeted chromatin histone marks (H3K56ac and H4K12ac), which are induced by CS. Thus CS-induced genotoxic stress differentially affects the expression of epigenetic modulators that regulate transcription of target genes via DNA methylation and site-specific histone modifications. This may have implications in devising epigenetic-based therapies for COPD and lung cancer.

Indexed as

Epigenesis, GeneticGene Expression ProfilingAcetylationAnimalsBronchiChromatinDatabases, GeneticEpithelial CellsHistone AcetyltransferasesHistone CodeHistone DeacetylasesHistone-Lysine N-MethyltransferaseHistone MethyltransferasesHistonesHumansLungChromatinHistone AcetyltransferasesHistone DeacetylasesHistone-Lysine N-MethyltransferaseHistone MethyltransferasesHistoneschromatin modificationscigarette smokeCOPDepigeneticsepithelial cellslungs

Identifiers

PMID27793800
PMCPMC5206398
OpenAlexW2775863097

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.