Evidence map›Paper›PMID 25442699›Full record

ArticleParticle and fibre toxicology2014

Ultrafine carbon particle mediated cardiovascular impairment of aged spontaneously hypertensive rats.

Swapna Upadhyay, Tobias Stoeger, Leema George, Mette C Schladweiler, Urmila Kodavanti, Koustav Ganguly, Holger Schulz

Open access · goldAbstract read
In one paragraph

Article in Particle and fibre toxicology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.0field-weighted citation impact, top 16% 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

11 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Cardiovascular adaptations to particle inhalation exposure: molecular mechanisms of the toxicology.American journal of physiology. Heart and circulatory physiology · 2020
    Review
  5. Article
  6. Ambient air pollution and thrombosis.Particle and fibre toxicology · 2018
    Review
  7. In Utero Exposure to Fine Particulate Matter Causes Hypertension Due to Impaired Renal Dopamine D1 Receptor in Offspring.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2018
    Article
  8. Article
  9. Review
  10. Article
  11. 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

7 authors at 3 institutions in 3 countries.

Swapna UpadhyayInstitute of Lung Biology and Disease, Comprehensive Pneumology Center Helmholtz Zentrum München, German Research Center for Environmental Health, Munich, Germany. swapnaupadhyay@gmail.com.
Tobias StoegerInstitute of Lung Biology and Disease, Comprehensive Pneumology Center Helmholtz Zentrum München, German Research Center for Environmental Health, Munich, Germany. tobias.stoeger@helmholtz-muenchen.de.
Leema GeorgeSRM Research Institute, SRM University, Chennai, 603203, India. leema.g@res.srmuniv.ac.in.
Mette C SchladweilerEnvironmental Public Health Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina, NC, 27711, USA. Schladweiler.Mette@epamail.epa.gov.
Urmila KodavantiEnvironmental Public Health Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina, NC, 27711, USA. kodavanti.urmila@epa.gov.
Koustav GangulyInstitute of Lung Biology and Disease, Comprehensive Pneumology Center Helmholtz Zentrum München, German Research Center for Environmental Health, Munich, Germany. koustav.g@res.srmuniv.ac.in.
Holger SchulzInstitute of Lung Biology and Disease, Comprehensive Pneumology Center Helmholtz Zentrum München, German Research Center for Environmental Health, Munich, Germany. schulz@helmholtz-muenchen.de.
Helmholtz Zentrum München · DEEnvironmental Protection Agency · USSRM University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundStudies provide compelling evidences for particulate matter (PM) associated cardiovascular health effects. Elderly individuals, particularly those with preexisting conditions like hypertension are regarded to be vulnerable. Experimental data are warranted to reveal the molecular pathomechanism of PM related cardiovascular impairments among aged/predisposed individuals. Thus we investigated the cardiovascular effects of ultrafine carbon particles (UfCP) on aged (12-13 months) spontaneously hypertensive rats (SHRs) and compared the findings with our pervious study on adult SHRs (6-7 months) to identify age related predisposition events in cardiovascular compromised elderly individuals.

methodsAged SHRs were inhalation exposed to UfCP for 24 h (~180 μg/m³) followed by radio-telemetric assessment for blood pressure (BP) and heart rate (HR). Bronchoalveolar lavage (BAL) fluid cell differentials, interleukin 6 (IL-6) and other proinflammatory cytokines; serum C-reactive protein (CRP) and haptoglobin (HPT); and plasma fibrinogen were measured. Transcript levels of hemeoxygenase 1 (HO-1), endothelin 1 (ET1), endothelin receptors A, B (ETA, ETB), tissue factor (TF), and plasminogen activator inhibitor-1 (PAI-1) were measured in the lung and heart to assess oxidative stress, endothelial dysfunction and coagulation cascade.

resultUfCP exposed aged SHRs exhibited increased BP (4.4%) and HR (6.3%) on 1(st) recovery day paralleled by a 58% increase of neutrophils and 25% increase of IL-6 in the BAL fluid. Simultaneously higher CRP, HPT and fibrinogen levels in exposed SHRs indicate systemic inflammation. HO-1, ET1, ET-A, ET-B, TF and PAI-1 were induced by 1.5-2.0 folds in lungs of aged SHRs on 1(st) recovery day. However, in UfCP exposed adult SHRs these markers were up-regulated (2.5-6 fold) on 3(rd) recovery day in lung without detectable pulmonary/systemic inflammation.

conclusionsThe UfCP induced pulmonary and systemic inflammation in aged SHRs is associated with oxidative stress, endothelial dysfunction and disturbed coagulatory hemostasis. UfCP exposure increased BP and HR in aged SHRs rats which was associated with lung inflammation, and increased expression of inflammatory, vasoconstriction and coagulation markers as well as systemic changes in biomarkers of thrombosis in aged SHRs. Our study provides further evidence for potential molecular mechanisms explaining the increased risk of particle mediated cardiac health effects in cardiovascular compromised elderly individuals.

Indexed as

AgingAir PollutantsAnimalsAtmosphere Exposure ChambersCarbonCardiovascular DiseasesCardiovascular SystemCytokinesHeartHypertensionInflammation MediatorsInhalation ExposureLungMaleMyocardiumOxidative StressAir PollutantsCarbonCytokinesInflammation MediatorsParticulate Matter

Identifiers

PMID25442699
PMCPMC4410795
OpenAlexW2056495937

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.