The prenatal nicotine exposure leads to epigenetic alterations in nervous system signaling genes in the rat [MeDIP]
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE253594 | GEO | 2024/04/26
REPOSITORIES: GEO
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Project description:Background. Prenatal exposure to nicotine has been documented to impose numerous deleterious effects on fetal development. However, the epigenetic changes promoted by nicotine exposure on germ cell are still not well understood. Objectives. In this study, we focused on elucidating the impact of prenatal nicotine exposure on regulatory epigenetic mechanisms important for the germ cells development. Objectives. In this study, we focused on elucidating the impact of prenatal nicotine exposure on regulatory epigenetic mechanisms important for the germ cells development.
2024-04-26 | GSE253595 | GEO
Project description:Here, we investigated whether prenatal exposure to nicotine alters kidney glomerular mass and genome-wide gene expression profiles in two genetically distant strains of rats, namely spontaneously hypertensive rats (SHR) and Brown Norway (BN) rats. Nicotine or saline were administered to BN and SHR dams via osmotic pumps throughout gestation. Kidneys from 9-week-old male offspring were studied. Equal amounts of RNA from individual animals were pooled within each of the four experimental groups SHR (nicotine: n=13; saline: n=12) and BN (nicotine: n=12; saline: n=12) and hybridized with the Rat RAE-230a GeneChip (Affymetrix).
2012-12-25 | E-GEOD-29677 | biostudies-arrayexpress
Project description:Here, we investigated whether prenatal exposure to nicotine alters kidney glomerular mass and genome-wide gene expression profiles in two genetically distant strains of rats, namely spontaneously hypertensive rats (SHR) and Brown Norway (BN) rats. Nicotine or saline were administered to BN and SHR dams via osmotic pumps throughout gestation. Kidneys from 9-week-old male offspring were studied.
2012-12-25 | GSE29677 | GEO
Project description:We used microarrays to determine the effect of prenatal nicotine exposure on gene expression profiles in the striatum of adolescent rats. We found a number of immediate early genes to be differentially expressed due to food-restriction. We compared control (n=8), nicotine exposed (n=7) and a group of animals matched to the food intake of nicotine exposed animals (n=10) to identify gene expression changes associated with prenatal nicotine exposure
2013-09-06 | E-GEOD-50607 | biostudies-arrayexpress
Project description:Perinatal smoke/nicotine exposure alters lung development and causes asthma in exposed offspring, transmitted transgenerationally. The mechanism underlying the transgenerational inheritance of perinatal smoke/nicotine-induced asthma remains unknown, but germline epigenetic modulations may play a role. Using a well-established rat model of perinatal nicotine-induced asthma, we determined the DNA methylation pattern of spermatozoa of F1 rats exposed perinatally to nicotine in F0 gestation. To identify differentially methylated regions (DMRs), reduced representation bisulfite sequencing was performed on spermatozoa of F1 litters. The top regulated gene body and promoter DMRs were tested for lung gene expression levels, and key proteins involved in lung development and repair were determined. The overall CpG methylation in F1 sperms across gene bodies, promoters, 5’UTRs, exons, introns, and 3’UTRs was not affected by nicotine exposure. However, the methylation levels were different between the different genomic regions. 81 CpG sites, 16 gene bodies, and 3 promoter regions were differentially methylated. Gene enrichment analysis of DMRs revealed pathways involved in oxidative stress, nicotine response, alveolar and brain development, and cellular signaling. Among the DMRs, Dio1 and Nmu were the most hypermethylated and hypomethylated genes, respectively. Gene expression analysis showed that the mRNA expression and DNA methylation were incongruous. Key proteins involved in lung development and repair were significantly different (FDR < 0.05) between the nicotine and placebo-treated groups. Our data show that DNA methylation is remodeled in offspring spermatozoa upon perinatal nicotine exposure. These epigenetic alterations may play a role in transgenerational inheritance of perinatal smoke/nicotine induced asthma.
2021-05-17 | GSE173898 | GEO
Project description:Neural tube defects (NTD) occur in 3000 births per year in the US. Several risk factors have been proposed for NTDs including both first hand and passive smoking during the periconceptual period. Previously we reported an increased frequency of cervical region NTD in a chicken model of prenatal nicotine exposure (Bohn, Humphrey et al. 2014; Humprey, Bohn et al. 2014). Here, we will reveal the mechanisms of the insult. The specific aims include: 1) Evaluation of the gene expression changes in the chicken model of nicotine exposure that we developed previosly. Such genome-wide analysis of the expression allows to collect very detailed data regarding the drug impact. To our knowlidge, comparable analysis of nicotine induced changes in gene expression during development of any species has never been conducted. 2) Evaluation of nicotine induced alterations in tadpoles (Xenopus tropica). The frogs will be treated in a manner similar to chicken (the same drug doses and a matched time of sacrifice) and analyzed both histologically and for gene expression. Incorporation of a different group of vertebrates in this study is essential for dissecting the evolutionary conserved role this pathway of interest in development which is another strong aspect of this proposal. We believe, that our comparative approach will allow more effective extrapolation of data from animal models to humans and better understanding of the evolutionary process. Nicotine is one of the most common developmental insults in humans. The consequences of this exposure are well-documented. However, the affected pathways are unknown. The identification of the mechanisms of nicotine induced alterations proposed here is vital for development of better treatment strategies.
2020-09-11 | GSE103703 | GEO
Project description:We used microarrays to determine the effect of prenatal nicotine exposure on gene expression profiles in the striatum of adolescent rats. We found a number of immediate early genes to be differentially expressed due to food-restriction.
2013-09-06 | GSE50607 | GEO
Project description:Background: How prenatal smoke exposure affects DNA methylation leading to atopic disorders remains to be addressed. Epigenetic biomarkers informative of prenatal smoke exposure and atopic disorders are wanting. Since most children suffering from atopic dermatitis (AD) continue to develop asthma later in life, we explored whether prenatal smoke exposure e induces DNA methylation and searched for predictive epigenetic biomarkers for smoke related atopic disorders. Methods: Methylation differences associated with smoke exposure were screened by Illumina methylation panel for children from the Taiwan birth panel study cohort initially. Information about development of atopic dermatitis (AD) and risk factors were collected. Cord blood cotinine levels were measured to represent prenatal smoke exposure. CpG loci that demonstrated a statistically significant difference in methylation were validated by methylation-dependent fragment separation (MDFS). Differential methylation in three genes (TSLP, GSTT1, and CYB5R3) was identified through the screen and their functions were investigated. Results: Among these, only thymic stromal lymphopoietin (TSLP) gene displayed significant difference in promoter methylation percentage after being validated by MDFS (p=0.029). TSLP gene was further investigated in a larger sample of 92 children from the cohort. Methylation status of the TSLP 5′-CpG island (CGI) was found to be significantly associated with prenatal smoke exposure (OR=3.59, 95%CI=1.49-8.64; cotinine level 0.10 ng/ml, sensitivity= 77%; specificity = 61%) and with AD (OR=4.77, 95%CI=1.47-15.53). The degree of TSLP 5′CGI methylation inversely correlated with TSLP protein expression levels (per unit: β=－6.69 ng/ml; 95% CIs, －12.80~－0.59; p=0.032). Conclusions: The effect of prenatal tobacco smoke exposure on the risk for AD may be mediated through DNA methylation. Cord blood methylated TSLP 5′CGI may be a potential epigenetic biomarker for environmentally-related atopic disorders. The buffy coat and plasma samples were separated and stored at −80°C. DNA (100 ng-500 ng) was extracted from cord white blood cells. Microarrays have been performed to investigate fourteen samples, which were classified as two groups according to cotinine exposure dosage (7 versus 7 : high exposure verses low exposure).
2013-12-31 | E-GEOD-35222 | biostudies-arrayexpress
Project description:The long-term objective of this project is to establish roles played in development and function of the immune system by nicotinic acetylcholine receptors (nAChR) and exposure to the tobacco alkaloid, nicotine. The planned gene chip studies will allow us to assess effects of nicotine exposure on gene expression in a model T cell line, and the findings are expected to help direct further efforts. One of the biomedically-relevant hypotheses of this project is that tobacco use and nicotine exposure affect immune system development. To establish effects of nicotine exposure on gene expression in the CEM model T cell line. Immune system nAChR acting as ion channels or via novel signaling cascades mediate their effects on T cell development by altering expression of genes involved in T cell receptor rearrangements, cytokine expression, and cell death/survival decisions. CEM cells will be treated for one hour or one day with an effective dose of nicotine or with the same medium change but in the absence of nicotine. Keywords: nicotine, T cell line
2008-04-12 | GSE11142 | GEO
Project description:Our laboratory previous research confirmed that nicotine in cigarette smoke causes apoptosis in germ cells in the testis and it will increase the formation of autophagosomes in the cytoplasm of testicular stromal cells. In addition, nicotine, the main toxic substance in cigarette smoke, also affects telomerase activity of spermatogenic cells, shortens telomere length, and causes structural damage of chromosomes. It is worth noting that after nicotine treatment, the expression of proteins involved in cytoskeleton regulation and energy metabolism in mouse testis was significantly up-regulated, and the sperm motility of mice was improved after nicotine treatment. To investigate the underlying mechanism, C57BL/6J mice were divided into control and nicotine treated groups. Next generation RNA sequencing and bio-informatics analysis were carried out to analysis the effects of nicotine on the RNA profile of mice spermatozoa. The results of RNA-Seq showed that the number of reads in the control group was 2089729, and the number of reads in the nicotine-treated group was 1739093, and a total of 8699 transcripts were obtained. Expression level of some pathways remarkably changed after nicotine treatment.This experimental study are helpful to understand the mechanism of the effect of nicotine on sperm and help us to provide a way to study the effection of patern nicotine exposure on offspring development.
2021-07-31 | GSE155145 | GEO