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.
2021-08-18 | GSE94347 | GEO
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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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:Mass spectrometry-based proteomic strategies can profile the expression level of proteins in response to external stimuli. Nicotine affects diverse cellular pathways, however, the nicotine-induced alterations on the global proteome across human cell lines have not been fully elucidated. We measured perturbations in protein levels resulting from nicotine treatment in four cell lines - HEK, HeLa, PaSC, and SH-SY5Y- in a single experiment using tandem mass tags (TMT10-plex) and high-resolution mass spectrometry. We quantified 8590 proteins across all cell lines. Of these, nicotine increased the abundance of 31 proteins 1.5-fold or greater in all cell lines. Likewise, considering proteins with altered levels in at least 3 of the 4 cell lines, 64 were up-regulated, while 1 was down-regulated. Gene ontology analysis revealed that ~40% of these proteins were membrane-bound, and functioned in transmembrane signaling and receptor activity. We highlighted proteins, including APP, APLP2, LAPTM4B, and NCOA4, which were dysregulated by nicotine in all cell lines investigated and may have implications in downstream signaling pathways, particularly autophagy. Using the outlined methodology, studies in additional (including primary) cell lines will provide further evidence that alterations in the levels of these proteins are indeed a general response to nicotine and thereby merit further investigation.
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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.
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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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