Single-Cell RNA-Sequencing of Human Embryonic Stem Cell Differentiation Delineates Adverse Effects of Nicotine on Embryonic Development
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA516340 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8479160.fastq.gz | Fastqsanger.gz | |||
| SRR8479161.fastq.gz | Fastqsanger.gz | |||
| SRR8479158.fastq.gz | Fastqsanger.gz | |||
| SRR8479159.fastq.gz | Fastqsanger.gz |
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Project description:Nicotine, the main constituent of tobacco, is highly detrimental to the developing fetus by increasing the risk of gestational complications and organ disorders. The effects of nicotine on human embryonic development and related mechanisms, however, remain largely unresolved. Here, we performed single-cell RNA-sequencing (scRNA-seq) of human embryonic stem cell (hESC)-derived embryoid body (EB) in the presence or absence of nicotine. Nicotine induced lineage-specific responses and dysregulated cell-to-cell communication in EBs, shedding light on the adverse effects of nicotine on human embryonic development. Additionally, nicotine reduced cell viability, increased reactive oxygen species (ROS), and altered cell cycling in EBs. Abnormal Ca2+ signaling was found in muscle cells upon nicotine exposure and verified in hESC-derived cardiomyocytes. Consequently, our scRNA-seq data suggests direct adverse effects of nicotine on hESC differentiation at the single-cell level and offers new method for evaluating drug and environmental toxicity on human embryonic development in utero.
2019-01-22 | GSE125416 | GEO
Project description:Nicotine, the main chemical constituent of tobacco, is highly detrimental to the developing fetus by increasing the risk of gestational complications and organ disorders. The effects of nicotine on human embryonic development and related mechanisms, however, remain poorly understood. Here, we performed single-cell RNA sequencing (scRNA-seq) of human embryonic stem cell (hESC)-derived embryoid body (EB) in the presence or absence of nicotine. Nicotine-induced lineage-specific responses and dysregulated cell-to-cell communication in EBs, shedding light on the adverse effects of nicotine on human embryonic development. In addition, nicotine reduced cell viability, increased reactive oxygen species (ROS), and altered cell cycling in EBs. Abnormal Ca2+ signaling was found in muscle cells upon nicotine exposure, as verified in hESC-derived cardiomyocytes. Consequently, our scRNA-seq data suggest direct adverse effects of nicotine on hESC differentiation at the single-cell level and offer a new method for evaluating drug and environmental toxicity on human embryonic development in utero.
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Project description:The in utero environment is a critical determinant of the immediate and future health of the developing fetus. Two of the most commonly used drugs during pregnancy are alcohol and nicotine. While prolonged gestational exposure to alcohol or nicotine has been associated with a range of adverse outcomes in the offspring, the consequences of exposure during early gestation only are less well understood. Here, we use mouse models of relatively moderate early gestational ethanol or nicotine exposure to profile gene expression in whole male embryos at 9.5 days post coitum using an Illumina microarray.
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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: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
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