Evidence map›Paper›PMID 26113123›Full record

ArticleParticle and fibre toxicology2015

Acute and subchronic exposure to air particulate matter induces expression of angiotensin and bradykinin-related genes in the lungs and heart: Angiotensin-II type-I receptor as a molecular target of particulate matter exposure.

Octavio Gamaliel Aztatzi-Aguilar, Marisela Uribe-Ramírez, José Antonio Arias-Montaño, Olivier Barbier, Andrea De Vizcaya-Ruiz

Open access · goldAbstract readComparative Study
In one paragraph

Article in Particle and fibre toxicology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 20% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. PMToxics · 2024
    Article
  6. Article
  7. Association between long-term exposure to PMFrontiers in public health · 2024
    Article
  8. Article
  9. Air pollution and respiratory infections: the past, present, and future.Toxicological sciences : an official journal of the Society of Toxicology · 2023
    Review
  10. Review
  11. Association Between Long-term Ambient PMAmerican journal of kidney diseases : the official journal of the National Kidney Foundation · 2022
    Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. The impact of outdoor air pollution on COVID-19: a review of evidence fromEuropean respiratory review : an official journal of the European Respiratory Society · 2021
    Review
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 1 country.

Octavio Gamaliel Aztatzi-AguilarDepartamento de Toxicología, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Avenida Instituto Politécnico Nacional, 2508, México D. F, CP. 07360, Mexico. gammaztatzi@gmail.com.
Marisela Uribe-RamírezDepartamento de Toxicología, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Avenida Instituto Politécnico Nacional, 2508, México D. F, CP. 07360, Mexico. tmuribe@yahoo.com.
José Antonio Arias-MontañoDepartamento de Fisiología, Neurociencias y Biofísica, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Avenida Instituto Politécnico Nacional, 2508, México D. F, C.P. 07360, Mexico. jaarias@fisio.cinvestav.mx.
Olivier BarbierDepartamento de Toxicología, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Avenida Instituto Politécnico Nacional, 2508, México D. F, CP. 07360, Mexico. obarbier@cinvestav.mx.
Andrea De Vizcaya-RuizDepartamento de Toxicología, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Avenida Instituto Politécnico Nacional, 2508, México D. F, CP. 07360, Mexico. avizcaya@cinvestav.mx.
Instituto Politécnico Nacional · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundParticulate matter (PM) adverse effects on health include lung and heart damage. The renin-angiotensin-aldosterone (RAAS) and kallikrein-kinin (KKS) endocrine systems are involved in the pathophysiology of cardiovascular diseases and have been found to impact lung diseases. The aim of the present study was to evaluate whether PM exposure regulates elements of RAAS and KKS.

methodsSprague-Dawley rats were acutely (3 days) and subchronically (8 weeks) exposed to coarse (CP), fine (FP) or ultrafine (UFP) particulates using a particulate concentrator, and a control group exposed to filtered air (FA). We evaluated the mRNA of the RAAS components At1, At2r and Ace, and of the KKS components B1r, B2r and Klk-1 by RT-PCR in the lungs and heart. The ACE and AT1R protein were evaluated by Western blot, as were HO-1 and γGCSc as indicators of the antioxidant response and IL-6 levels as an inflammation marker. We performed a binding assay to determinate AT1R density in the lung, also the subcellular AT1R distribution in the lungs was evaluated. Finally, we performed a histological analysis of intramyocardial coronary arteries and the expression of markers of heart gene reprogramming (Acta1 and Col3a1).

resultsThe PM fractions induced the expression of RAAS and KKS elements in the lungs and heart in a time-dependent manner. CP exposure induced Ace mRNA expression and regulated its protein in the lungs. Acute and subchronic exposure to FP and UFP induced the expression of At1r in the lungs and heart. All PM fractions increased the AT1R protein in a size-dependent manner in the lungs and heart after subchronic exposure. The AT1R lung protein showed a time-dependent change in subcellular distribution. In addition, the presence of AT1R in the heart was accompanied by a decrease in HO-1, which was concomitant with the induction of Acta1 and Col3a1 and the increment of IL-6. Moreover, exposure to all PM fractions increased coronary artery wall thickness.

conclusionWe demonstrate that exposure to PM induces the expression of RAAS and KKS elements, including AT1R, which was the main target in the lungs and the heart.

Indexed as

ActinsAnimalsAntioxidantsCollagen Type IIICytokinesGene Expression RegulationInhalation ExposureKallikrein-Kinin SystemLungMyocardiumParticle SizeParticulate MatterRats, Sprague-DawleyRenin-Angiotensin SystemRNA, MessengerTime FactorsActinsAntioxidantsCOL3A1 protein, ratCollagen Type IIICytokinesParticulate MatterRNA, Messenger

Identifiers

PMID26113123
PMCPMC4482198
OpenAlexW1797360749

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.