Cited by 56Neurogenesis and neuroplasticity mechanismsAir Quality and Health ImpactsFetal and Pediatric Neurological Disorders

Exposure to fine and ultrafine particulate matter during gestation alters postnatal oligodendrocyte maturation, proliferation capacity, and myelination

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Klocke, Carolyn, Allen, Joshua L., Sobolewski, Marissa, Blum, Jason L., Zelikoff, Judith T., Cory-Slechta, Deborah A.·2018·NeuroToxicology

Abstract

Accumulating studies indicate that the brain is a direct target of air pollution exposure during the fetal period. We have previously demonstrated that exposure to concentrated ambient particles (CAPs) during gestation produces ventriculomegaly, periventricular hypermyelination, and enlargement of the corpus callosum (CC) during postnatal development in mice. This study aimed to further characterize the cellular basis of the observed hypermyelination and determine if this outcome, among other effects, persisted as the brain matured. Analysis of CC-1+ mature oligodendrocytes in the CC at postnatal days (PNDs) 11-15 suggest a premature maturational shift in number and proportion of total cells in prenatally CAPs-exposed males and females, with no overall change in total CC cellularity. The overall number of Olig2+ lineage cells in the CC was not affected in either sex at the same postnatal timepoint. Assessment of myelin status at early brain maturity (PNDs 57-61) revealed persistent hypermyelination in CAPs-exposed animals of both sexes. In addition, ventriculomegaly was persistent in CAPs-treated females, with possible amelioration of ventriculomegaly in CAPs-exposed males. When oligodendrocyte precursor cell (OPC) pool status was analyzed at PNDs 57-61, there were significant CAPs-induced alterations in cycling Ki67+/Olig2+ cell number and proportion of total cells in the female CC. Total CC cellularity was slightly elevated in CAPs-exposed males at PNDs 57-61. Overall, these data support a growing body of evidence that demonstrate the vulnerability of the developing brain to environmental insults such as ambient particulate matter. The sensitivity of oligodendrocytes and myelin, in particular, to such an insult warrants further investigation into the mechanistic underpinnings of OPC and myelin disruption by constituent air pollutants.

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Cited by

Sorted by citations

Authors
Klocke, C., Allen, J. L., Sobolewski, M., Blum, J. L., Zelikoff, J. T., & Cory-Slechta, D. A.
Affiliations
  • University of Rochester Medicine (US)
  • New York University (US)
Corresponding author
Klocke, Carolyn
Venue
NeuroToxicology
Publisher
Elsevier BV
Published
2018-03
Volume
65
Pages
196-206
ISSN
0161-813X (ISSN-L)
OpenAlex
W2766427800
Cited by
56
References
7
Citations by year
2026: 3 · 2025: 6 · 2024: 4 · 2023: 6 · 2022: 9 · 2021: 8 · 2020: 11 · 2019: 6 · 2018: 3
FWCI
2.32
Type
journal article
Language
en
Open access
Locations
  • NeuroToxicology (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Environmental Health Sciences (P30 ES001247, R01 ES025541, T32 ES07026, P30 ES000260)
  • March of Dimes (21-F12-13)
Topics
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Air Quality and Health Impacts
  • Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Fetal and Pediatric Neurological Disorders
Keywords
PM2.5, ultrafine particles, air pollution, prenatal exposure, gestation, oligodendrocyte maturation, oligodendrocyte precursor cells, myelination, hypermyelination, ventriculomegaly, corpus callosum, Olig2, Ki-67, brain development, sex differences, environmental neurotoxicity
MeSH terms
Animals, Cell Differentiation, Female, Hydrocephalus, Male, Myelin Sheath, Oligodendroglia, Particle Size, Pregnancy, Prenatal Exposure Delayed Effects, Sex Factors, Cell Proliferation, Mice, Particulate Matter

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