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Cited by 69Air Quality and Health ImpactsCardiac Fibrosis and RemodelingCardiovascular Function and Risk Factors

In Utero Particulate Matter Exposure Produces Heart Failure, Electrical Remodeling, and Epigenetic Changes at Adulthood

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Tanwar, Vineeta, Gorr, Matthew W., Velten, Markus, Eichenseer, Clayton M., Long, Victor P., Bonilla, Ingrid M., Shettigar, Vikram, Ziolo, Mark T. +4 more·2017·Journal of the American Heart Association
DOI 10.1161/jaha.117.005796PMC PMC5533043
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Abstract

Background: Particulate matter (PM; PM 2.5 [PM with diameters of <2.5 μm]) exposure during development is strongly associated with adverse cardiovascular outcomes at adulthood. In the present study, we tested the hypothesis that in utero PM 2.5 exposure alone could alter cardiac structure and function at adulthood. Methods and Results: Female FVB mice were exposed either to filtered air or PM 2.5 at an average concentration of 73.61 μg/m 3 for 6 h/day, 7 days/week throughout pregnancy. After birth, animals were analyzed at 12 weeks of age. Echocardiographic (n=9–10 mice/group) and pressure‐volume loop analyses (n=5 mice/group) revealed reduced fractional shortening, increased left ventricular end‐systolic and ‐diastolic diameters, reduced left ventricular posterior wall thickness, end‐systolic elastance, contractile reserve ( dP /dt max /end‐systolic volume), frequency‐dependent acceleration of relaxation), and blunted contractile response to β‐adrenergic stimulation in PM 2.5 ‐exposed mice. Isolated cardiomyocyte (n=4–5 mice/group) function illustrated reduced peak shortening, ± dL / dT , and prolonged action potential duration at 90% repolarization. Histological left ventricular analyses (n=3 mice/group) showed increased collagen deposition in in utero PM 2.5 ‐exposed mice at adulthood. Cardiac interleukin ( IL) ‐6, IL ‐1ß, collagen‐1, matrix metalloproteinase ( MMP ) 9, and MMP 13 gene expressions were increased at birth in in utero PM 2.5 ‐exposed mice (n=4 mice/group). In adult hearts (n=5 mice/group), gene expressions of sirtuin (Sirt) 1 and Sirt2 were decreased, DNA methyltransferase (Dnmt) 1, Dnmt3a, and Dnmt3b were increased, and protein expression (n=6 mice/group) of Ca 2+ ‐ATPase, phosphorylated phospholamban, and Na + /Ca 2+ exchanger were decreased. Conclusions: In utero PM 2.5 exposure triggers an acute inflammatory response, chronic matrix remodeling, and alterations in Ca 2+ handling proteins, resulting in global adult cardiac dysfunction. These results also highlight the potential involvement of epigenetics in priming of adult cardiac disease.

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  • In utero exposure to PM2.5 in mice produced adverse cardiac phenotypes at 12 weeks, including reduced fractional shortening, increased left ventricular end-systolic and end-diastolic diameters, reduced left ventricular posterior wall thickness, end-systolic elastance, contractile reserve, frequency-dependent acceleration of relaxation, and blunted contractile response to β-adrenergic stimulation.

    “Investigators demonstrated several adverse phenotypes in exposed offspring evaluated at 12 weeks, including reduced fractional shortening, increased left ventricular end-systolic and end-diastolic diameters, reduced left ventricular posterior wall thickness, end-systolic elastance, contractile reserve, frequency-dependent acceleration of relaxation, and blunted contractile response to β-adrenergic”

    From Air pollution and children’s health—a review of adverse effects associated with prenatal exposure from fine to ultrafine particulate matter (2021) · cites this paper as [65]

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  • Acute inflammatory markers, alterations in Ca2+ handling proteins, and changes in protein expression of DNA methyltransferases were marked in PM2.5-exposed offspring, suggesting a role of epigenetic changes in priming heart disease risk.

    “Acute inflammatory markers, alterations in Ca2+ handling proteins, and changes in protein expression of DNA methyltransferases were also marked in the exposed group, suggesting the role of epigenetic changes in priming heart disease risk.”

    From Air pollution and children’s health—a review of adverse effects associated with prenatal exposure from fine to ultrafine particulate matter (2021) · cites this paper as [65]

    The Results report increased inflammatory-marker mRNA in newborn mice, altered Ca2+-handling proteins in adult hearts, and increased DNA methyltransferase expression in adult hearts after in utero PM2.5 exposure. The Abstract Conclusions suggest potential epigenetic involvement in adult cardiac disease. However, the DNA methyltransferase measurements were of mRNA, not protein expression as the claim states. (LLM, conf=0.91)

    Experimental — accuracy not yet measured

  • Similar average levels were recorded for concentrated PM2.5 from the Columbus, OH region.

    “Similar average levels were recorded for concentrated PM2.5 from the Columbus, OH region [64–66].”

    From Air pollution and children’s health—a review of adverse effects associated with prenatal exposure from fine to ultrafine particulate matter (2021) · cites this paper as [65]

  • Histological assessment showed increased collagen deposition in offspring exposed in utero to PM2.5, confirming findings from Gorr et al.

    “Moreover, histological assessment showed increase collagen deposition in exposed offspring, confirming findings from Gorr et al. [64, 65].”

    From Air pollution and children’s health—a review of adverse effects associated with prenatal exposure from fine to ultrafine particulate matter (2021) · cites this paper as [65]

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Cited by

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Authors
Tanwar, V., Gorr, M. W., Velten, M., Eichenseer, C. M., Long, V. P., Bonilla, I. M., Shettigar, V., Ziolo, M. T., Davis, J. P., Baine, S. H., Carnes, C. A., & Wold, L. E.
Affiliations
  • The Ohio State University (US)
  • University of Bonn (DE)
Corresponding author
Wold, Loren E.
ORCID
Venue
Journal of the American Heart Association
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2017-04-05
Volume
6
Issue
4
ISSN
2047-9980 (ISSN-L)
DOI
10.1161/jaha.117.005796
PMC
PMC5533043
OpenAlex
W2607328229
Cited by
69
References
3
Citations by year
2026: 2 · 2025: 7 · 2024: 6 · 2023: 4 · 2022: 8 · 2021: 12 · 2020: 5 · 2019: 15 · 2018: 6 · 2017: 3
FWCI
4.28
Type
journal article
Language
en
Open access
Licence
cc-by-nc
Locations
  • Journal of the American Heart Association (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • National Institute on Aging (R01AG057046)
  • National Heart, Lung, and Blood Institute (R01HL139348)
  • National Institute of Nursing Research (R01NR012618)
  • National Institute of Environmental Health Sciences (R01ES019923)
Topics
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Air Quality and Health Impacts
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
Keywords
particulate matter, PM2.5, prenatal air pollution exposure, heart failure, cardiac remodeling, electrical remodeling, epigenetic modifications, DNA methylation, sirtuins, calcium handling, cardiomyocyte contractility, cardiac inflammation, extracellular matrix remodeling, phospholamban, Na+/Ca2+ exchanger, FVB mice, left ventricular function
MeSH terms
DNA (Cytosine-5-)-Methyltransferase 1, DNA Methyltransferase 3A, DNA Methyltransferase 3B, Phospholamban, Action Potentials, Calcium-Transporting ATPases, Age Factors, Animals, Animals, Newborn, Arrhythmias, Cardiac, Calcium-Binding Proteins, DNA (Cytosine-5-)-Methyltransferases, Female, Gestational Age, Heart Failure, Heart Rate, Particle Size, Phosphorylation, Pregnancy, Prenatal Exposure Delayed Effects, Ventricular Function, Left, Maternal Exposure, Inhalation Exposure, Sodium-Calcium Exchanger, Ventricular Remodeling, Myocytes, Cardiac, Epigenesis, Genetic, Mice, Particulate Matter, Sirtuin 1, Sirtuin 2, Atrial Remodeling

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