Evidence map›Paper›PMID 28579250›Full record

ArticleToxicology and applied pharmacology2017

DNA methylation of extracellular matrix remodeling genes in children exposed to arsenic.

Tania Gonzalez-Cortes, Rogelio Recio-Vega, Robert Clark Lantz, Binh T Chau

Open access · greenAbstract read
In one paragraph

Article in Toxicology and applied pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 2 pooled it
1.1field-weighted citation impact, top 23% 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

13 citing papers in PubMed, 2 syntheses or guidelines pooled it, 24 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  7. Review
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  11. Impact of prenatal arsenic exposure on chronic adult diseases.Systems biology in reproductive medicine · 2018
    Review
  12. Article
  13. Article
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

4 authors at 2 institutions in 2 countries.

Tania Gonzalez-CortesDepartment of Environmental Health, Biomedical Research Center, School of Medicine, University of Coahuila, Torreon, Coahuila, Mexico.
Rogelio Recio-VegaDepartment of Environmental Health, Biomedical Research Center, School of Medicine, University of Coahuila, Torreon, Coahuila, Mexico. Electronic address: rogeliorecio@uadec.edu.mx.
Robert Clark LantzDepartment of Cellular and Molecular Medicine, University of Arizona, Tucson, AZ, United States; Southwest Environmental Health Science Center, University of Arizona, Tucson, AZ, United States.
Binh T ChauDepartment of Cellular and Molecular Medicine, University of Arizona, Tucson, AZ, United States.
Universidad Autónoma de Coahuila · MXUniversity of Arizona · US

Funding

TRANSPORT OF TRACE METALS IN A POLLUTED AQUIFERP42ES004940 · NIEHS · UNIVERSITY OF ARIZONA · PI Xinxin Ding · 1990 to 2026
$68.1M
SOUTHWEST ENVIRONMENTAL HEALTH SCIENCES CENTERP30ES006694 · NIEHS · UNIVERSITY OF ARIZONA · PI DEAN BILLHEIMER · 1994 to 2026
$36.7M
NIEHS NIH HHS P30 ES006694NIEHS NIH HHS P42 ES004940
6 · The paper itself

Abstract

Several novel mechanistic findings regarding to arsenic's pathogenesis has been reported and some of them suggest that the etiology of some arsenic induced diseases are due in part to heritable changes to the genome via epigenetic processes such as DNA methylation, histone maintenance, and mRNA expression. Recently, we reported that arsenic exposure during in utero and early life was associated with impairment in the lung function and abnormal receptor for advanced glycation endproducts (RAGE), matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1) sputum levels. Based on our results and the reported arsenic impacts on DNA methylation, we designed this study in our cohort of children exposed in utero and early childhood to arsenic with the aim to associate DNA methylation of MMP9, TIMP1 and RAGE genes with its protein sputum levels and with urinary and toenail arsenic levels. The results disclosed hypermethylation in MMP9 promotor region in the most exposed children; and an increase in the RAGE sputum levels among children with the mid methylation level; there were also positive associations between MMP9 DNA methylation with arsenic toenail concentrations; RAGE DNA methylation with iAs, and %DMA; and finally between TIMP1 DNA methylation with the first arsenic methylation. A negative correlation between MMP9 sputum levels with its DNA methylation was registered. In conclusion, arsenic levels were positive associated with the DNA methylation of extracellular matrix remodeling genes;, which in turn could modifies the biological process in which they are involved causing or predisposing to lung diseases.

Indexed as

Age FactorsArsenicArsenic PoisoningChildDNA MethylationExtracellular MatrixFemaleGenetic MarkersHumansMaleMaternal ExposureMatrix Metalloproteinase 9NailsPregnancyPrenatal Exposure Delayed EffectsPromoter Regions, GeneticAGER protein, humanArsenicGenetic MarkersMatrix Metalloproteinase 9MMP9 protein, humanReceptor for Advanced Glycation End ProductsTIMP1 protein, humanTissue Inhibitor of Metalloproteinase-1Water Pollutants, ChemicalArsenicChildrenDNA methylationMMP9RAGETIMP1

Identifiers

PMID28579250
PMCPMC5806512
OpenAlexW2621153762

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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.