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Cited by 62Air Quality and Health ImpactsBirth, Development, and HealthRenin-Angiotensin System Studies

In utero exposure to ultrafine particles promotes placental stress-induced programming of renin-angiotensin system-related elements in the offspring results in altered blood pressure in adult mice

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Morales-Rubio, Russell A., Alvarado-Cruz, Isabel, Manzano-León, Natalia, Andrade-Oliva, Maria-de-los-Angeles, Uribe-Ramirez, Marisela, Quintanilla-Vega, Betzabet, Osornio-Vargas, Álvaro, De Vizcaya-Ruiz, Andrea·2019·Particle and Fibre Toxicology
DOI 10.1186/s12989-019-0289-1PMC PMC6350404
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Abstract

Exposure to particulate matter (PM) is associated with an adverse intrauterine environment, which can promote adult cardiovascular disease (CVD) risk. Ultrafine particles (UFP) (small size and large surface area/mass ratio) are systemically distributed, induce inflammation and oxidative stress, and have been associated with vascular endothelial dysfunction and arterial vasoconstriction, increasing hypertension risk. Placental stress and alterations in methylation of promoter regions of renin-angiotensin system (RAS)-related elements could be involved in UFP exposure-related programming of hypertension. We investigated whether in utero UFP exposure promotes placental stress by inflammation and oxidative stress, alterations in hydroxysteroid dehydrogenase 11b-type 2 (HSD11B2) and programming of RAS-related elements, and result in altered blood pressure in adult offspring. UFP were collected from ambient air using an aerosol concentrator and physicochemically characterized. Pregnant C57BL/6J p un / p un female mice were exposed to collected UFP (400 μg/kg accumulated dose) by intratracheal instillation and compared to control (nonexposed) and sterile H 2 O (vehicle) exposed mice. Embryo reabsorption and placental stress by measurement of the uterus, placental and fetal weights, dam serum and fetal cortisol, placental HSD11B2 DNA methylation and protein levels, were evaluated. Polycyclic aromatic hydrocarbon (PAH) biotransformation (CYP1A1 and NQO1 (NAD(P)H dehydrogenase (quinone)1)) enzymes, inflammation and oxidative stress in placentas and fetuses were measured. Postnatal day (PND) 50 in male offspring blood pressure was measured. Methylation and protein expression of (RAS)-related elements, angiotensin II receptor type 1 (AT 1 R) and angiotensin I-converting enzyme (ACE) in fetuses and lungs of PND 50 male offspring were also assessed. In utero UFP exposure induced placental stress as indicated by an increase in embryo reabsorption, decreases in the uterus, placental, and fetal weights, and HSD11B2 hypermethylation and protein downregulation. In utero UFP exposure induced increases in the PAH-biotransforming enzymes, intrauterine oxidative damage and inflammation and stimulated programming and activation of AT 1 R and ACE, which resulted in increased blood pressure in the PND 50 male offspring. In utero UFP exposure promotes placental stress through inflammation and oxidative stress, and programs RAS-related elements that result in altered blood pressure in the offspring. Exposure to UFP during fetal development could influence susceptibility to CVD in adulthood.

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Authors
Morales-Rubio, R. A., Alvarado-Cruz, I., Manzano-León, N., Andrade-Oliva, M.-D.-L.-A., Uribe-Ramirez, M., Quintanilla-Vega, B., Osornio-Vargas, Á., & De Vizcaya-Ruiz, A.
Affiliations
  • Instituto Politécnico Nacional (MX)
  • University of Alberta (CA)
ORCID
Venue
Particle and Fibre Toxicology
Publisher
Springer Science and Business Media LLC
Published
2019-01-28
Volume
16
Issue
1
Pages
7-7
ISSN
1743-8977 (ISSN-L)
DOI
10.1186/s12989-019-0289-1
PMC
PMC6350404
OpenAlex
W2921219745
Cited by
62
References
81
Citations by year
2026: 7 · 2025: 5 · 2024: 11 · 2023: 5 · 2022: 11 · 2021: 12 · 2020: 7 · 2019: 4
FWCI
3.67
Type
journal article
Language
en
Open access
Licence
Locations
  • Particle and Fibre Toxicology (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, other-oa)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Consejo Nacional de Ciencia y Tecnología (CB-2011-167778 and CB-2016-286739)
  • Consejo Nacional de Ciencia y Tecnología, Mexico (Scholarship 403193)
  • REDCAM, Consejo Nacional de Ciencia y Tecnología, México
Topics
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Air Quality and Health Impacts
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
Keywords
ultrafine particles, prenatal exposure, renin-angiotensin system, 11β-hydroxysteroid dehydrogenase type 2, DNA methylation, epigenetic programming, blood pressure, hypertension, angiotensin II type 1 receptor, angiotensin-converting enzyme, polycyclic aromatic hydrocarbons, CYP1A1, NQO1, oxidative stress, inflammation, fetal cortisol, fetal lung, cardiovascular risk, prenatal air pollution exposure
MeSH terms
Animals, Animals, Newborn, Blood Pressure, Female, Hypertension, Peptidyl-Dipeptidase A, Lung, Male, Mice, Inbred C57BL, Particle Size, Placenta, Pregnancy, Prenatal Exposure Delayed Effects, Renin-Angiotensin System, Surface Properties, Oxidative Stress, Receptor, Angiotensin, Type 1, Fetal Development, Particulate Matter

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