Nicotine exposure declines quality of early embryos and disrupts placental structure by destabilizing Notch signaling pathway
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ABSTRACT:
PROVIDER: PRJNA774987 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16596661_1.fastq.gz | Fastqsanger.gz | |||
| SRR16596661_2.fastq.gz | Fastqsanger.gz | |||
| SRR16596662_1.fastq.gz | Fastqsanger.gz | |||
| SRR16596662_2.fastq.gz | Fastqsanger.gz | |||
| SRR16596663_1.fastq.gz | Fastqsanger.gz |
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Project description:Nicotine is a common environmental pollution which is diffused into the air in the form of cigarette smoke fumes. Due to its lipophilic nature, nicotine can rapidly transport through membrane barriers and spread throughout the body which leads to abnormalities in the human brain, heart and even the fatal. However, the effects of nicotine on early embryonic development remains elusive. In this study, we found that nicotine significantly affected early embryonic development with decreased blastocyst formation. In addition, embryos treated with nicotine caused increased level of ROS, DNA damage and cell apoptosis. By RNA sequencing analysis, we demonstrated that nicotine affected the expression of placental development genes. Consistently, we found that the placental development at E17.5 was impaired by nicotine exposure, with increased placental weight and disrupted placental structure. This was due to excessive activation of the Notch signaling pathway, since blocking Notch signal by DAPT treatment recovered abnormal placental weight and structure induced by nicotine exposure. We also observed that nicotine exposure could specifically cause promoter hypermethylation of Phlda2 (a maternally expressed imprinted gene associated with placental development) and lead to its abnormal expression. Overall, this study provides evidence that nicotine causes the declining quality of early embryo and leads to placental abnormalities related with over-activation of the Notch signaling pathway.
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Project description:Background. Prenatal nicotine exposure (PNE) has been shown to significantly impact fetal development, leading to various pathologies in adulthood, including those affecting the digestive system. Despite considerable attention from the scientific community on the health effects of nicotine consumption, the epigenetic effects of nicotine on the colon remain poorly understood. Objective, in this study, we analyzed the epigenetic effects of nicotine on the proximal colon.
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Project description:Background. Prenatal nicotine exposure (PNE) has been shown to significantly impact fetal development, leading to various pathologies in adulthood, including those affecting the digestive system. Despite considerable attention from the scientific community on the health effects of nicotine consumption, the epigenetic effects of nicotine on the colon remain poorly understood. Objective, in this study, we analyzed the epigenetic effects of nicotine on the proximal colon.
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Project description:The shotgun proteomics approach attempts to identify the proteins expressed by Paenarthrobacter (formerly Arthrobacter) nicotinovorans in the presence of nicotine by using nanoLCMSMS. A total of 792 non redundant proteins were identified when P. nicotinovorans was grown in on citrate, nicotine and citrate and nicotine as the only carbon source.
2018-01-25 | MSV000081968 | MassIVE
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.
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Project description:The long-term goal of this project is to establish whether and how chronic nicotine exposure affects nervous system function. The biological targets of nicotine action are diverse members of the superfamily of neurotransmitter-gated ion channels called nicotinic acetylcholine receptors (nAChR). nAChR play multiple, critical roles in chemical signaling throughout the brain and body. They also must be involved in nicotine dependence, which drives tobacco product use responsible for tremendous economic and personal costs. To define changes in gene expression induced by nicotine exposure in a model neuronal cell lines expressing at least two nicotinic receptor subtypes. Nicotine exposure exerst at least some of its effects on nervous system function by altering gene expression. Cells of the SH-SY5Y human neuroblastoma will be exposed to an efficacious dose of nicotine or to control medium for two different periods. Keywords: time-course
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