Dataset Information

Effect of Juvenile Environmental Tobacco Smoke Exposure on the Rat Frontal Cortex Neuroproteome

ABSTRACT: Exposure to secondhand tobacco smoke during early childhood has been linked with an increased risk for behavioral disorders, yet little is known regarding how brain development is impacted. Using an environmental tobacco smoke (ETS) passive inhalation model, this study assesses the neurodevelopmental impact of juvenile exposure during a critical period of frontal cortex development, specifically that of the rat orbital neocortex between postnatal days 8 and 22. Agnostic shotgun proteomics was employed to discern the biomolecular shift within this rapidly developing brain region that is responsible for higher-order behavioral control. The orbital cortex neuroproteome was assessed between ETS-exposed and room-air control animals employing a label-free shotgun approach with data-independent acquisition. Following protein roll-up, a total of X protein were found statistically altered in quantity out of Y total proteins identified. These results implicate a prominent shift within metabolic processes and synaptic organization related to excitatory and inhibitory neurotransmission. Findings derived from this dataset may further our understanding of how secondhand smoke exposure can perturb the orbital frontal cortex and result in developmental behavioral disorders.

INSTRUMENT(S): Synapt G2 HDMS

ORGANISM(S): Rattus Norvegicus (rat)

TISSUE(S): Brain

SUBMITTER: Andrew Ottens

LAB HEAD: Andrew K Ottens

PROVIDER: PXD007690 | Pride | 2020-05-26

REPOSITORIES: Pride

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Frontal Cortex Proteome Perturbation after Juvenile Rat Secondhand Smoke Exposure.

Lewis Liam S C LSC Muldoon Pretal P PP Pilaka Pallavi P PP Ottens Andrew K AK

Proteomics 20181206 24

Secondhand smoke remains a global concern for children's health. Epidemiological studies implicate exposure to secondhand smoke as a major risk factor for behavioral disorders, yet biological causation remains unclear. Model studies have mainly focused on secondhand smoke impacts to prenatal neurodevelopment, yet juvenile exposure represents a separate risk. Using ion mobility-enhanced data-independent mass spectrometry, the effect of juvenile secondhand smoke exposure on the prefrontal cortex, ...[more]

PMID: 30474317

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Project description:Passive smoke intake by pregnant women may have detrimental effects such as spontaneous abortion, lower birth weight, stillbirth, and reduced infant lung function. To extend our knowledge on molecular effects of tobacco smoke exposure in pregnancy, we analyzed transcriptome alterations in passive smokers (PS) and compared them to those in active smokers (AS). Using Illumina Expression Beadchip with 24,526 transcript probes, gene expression patterns were assayed in placentas from PS (N=25) exposed to environmental tobacco smoke (ETS) throughout pregnancy and non-exposed (NS) counterparts (N=35), and in cord blood cells from their newborns. The ETS exposure was evaluated by questionnaire disclosure and cotinine measurement in maternal and cord bloods. A total of 196 genes were significantly deregulated in placentas of PS compared to NS. These genes were primary associated with extracellular matrix, apoptosis, blood clotting, response to stress, embryonic morphogenesis, and lipid metabolism. Cord blood of newborns of PS displayed differential expression of 116 genes encoding mainly neuronal factors, regulators of immunologic response, and protooncogenes. Gene ontology analyses highlighted some important biological processes that might be associated with placental insufficiency and fetal growth restriction in PS, such as fatty acid catabolism, coagulation, regulation of growth, and response to steroid hormone stimulus. The study demonstrates that even low dose exposure to ETS during pregnancy leads to the significant deregulation of transcriptional regulation in placental and fetal cells. The data suggest the effect of ETS on the fetus is primary indirect, mediated via deregulation of placental functions. Comparison of PS and AS indicated that ETS exposure and active smoking in pregnancy partly employ the same molecular mechanisms. A total of 60 women who gave birth to a baby in the Faculty Hospital Motol (Czech Republic) were enrolled into the study approved by the local Institutional Review Board. The participants signed written informed consent and self-reported information on tobacco smoke exposure (type of exposure, number of cigarettes per day, exposure period) and life style during pregnancy (alcohol drinking, diet, area of residency etc.). Further, the women completed the questionnaire on pregnancy/delivery course (complications, diseases, medication, and delivery mode) and newborn characteristics (physical parameters, Apgar score) with the assistance of gynecologist. Only women without any health complications during pregnancy and their newborns without manifestation of pathological abnormalities were included in the study. Based on self-reported tobacco smoke exposure, the women were divided into two groups, non-smokers (NS, N=35) and passive smokers (PS, N=25). Former and active smokers were excluded from the study. Exposure to tobacco smoke was further evaluated by measurement of plasma cotinine levels in maternal peripheral blood and newborn cord blood using radioimmunoassay.

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