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Published on: December 14, 2014
Exposure to PM2.5 causes genetic changes in fetal rat cerebral cortex and hippocampus
Ming-Wei Chao1,2, Chin-Hua Yang3,4, Po-Ting Lin5
1Department of Bioscience Technology College of Science, Chung Yuan Christian University, Zhongli district, Taoyaun, 320, Taiwan.
Abstract:
PM2.5 travels along the respiratory tract and enters systemic blood circulation. Studies have shown that PM2.5 increases the incidence of various diseases not only in adults but also in newborn infants. It causes chronic inflammation in pregnant women and retards fetal development. In this study, pregnant rats were exposed to PM2.5 for extended periods of time and it was found that PM2.5 exposure increased immune cells in mother rats. In addition, cytokines and free radicals rapidly accumulated in the amniotic fluid and indirectly affected the fetuses. The authors collected cerebral cortex and hippocampus samples at E18 and analyzed changes of miRNA levels. Expression levels of cortical miR-6315, miR-3588, and miR-466b-5p were upregulated, and positively correlated with the genes Pkn2 (astrocyte migration), Gorab (neuritogenesis), and Mobp (allergic encephalomyelitis). In contrast, PM2.5 decreased expression of miR-338-5p and let-7e-5p, both related to mental development. Further, PM2.5 exposure increased miR-3560 and let-7b-5p in the hippocampus, two proteins that regulate genes Oxct1 and Lin28b that control ketogenesis and glycosylation, and neural cell differentiation, respectively. miR-99b-5p, miR-92b-5p, and miR-99a-5p were decreased, leading to reduced expression of Kbtbd8 and Adam11 which reduced cell mitosis, migration, and differentiation, and inhibited learning abilities and motor coordination of the fetus. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1412-1425, 2017.
Insights
Exposure to fine particulate matter (PM2.5) during pregnancy harms fetal brain development by altering microRNA levels. This can lead to reduced learning abilities and motor coordination in newborns.
Area of Science:
- Environmental Toxicology
- Developmental Biology
- Neuroscience
Background:
- Particulate Matter (PM2.5) exposure is linked to adverse health outcomes in adults and infants.
- Prenatal exposure to PM2.5 can cause chronic inflammation in pregnant women and impair fetal development.
- PM2.5 affects respiratory and systemic circulation, with potential impacts on fetal neurodevelopment.
Purpose of the Study:
- To investigate the effects of PM2.5 exposure on pregnant rats and their fetuses.
- To analyze changes in microRNA (miRNA) expression in the fetal brain following maternal PM2.5 exposure.
- To correlate altered miRNA levels with genes involved in neural development and function.
Main Methods:
- Pregnant rats were exposed to PM2.5.
- Immune cell counts, cytokine, and free radical levels in amniotic fluid were analyzed.
- Cerebral cortex and hippocampus samples were collected at E18 for miRNA and gene expression analysis.
Main Results:
- PM2.5 exposure increased maternal immune cells and altered amniotic fluid composition.
- Upregulation of cortical miRNAs (miR-6315, miR-3588, miR-466b-5p) correlated with genes for astrocyte migration and neuritogenesis.
- Downregulation of specific miRNAs (miR-338-5p, let-7e-5p, miR-99b-5p, miR-92b-5p, miR-99a-5p) was observed, impacting fetal learning, motor coordination, and neural cell differentiation.
Conclusions:
- Maternal PM2.5 exposure significantly impacts fetal brain development through miRNA dysregulation.
- Altered miRNA expression affects key genes involved in neurogenesis, cell migration, and differentiation.
- These molecular changes in the fetus may underlie developmental deficits in learning and motor coordination.
