Single-nucleus chromatin accessibility and RNA-seq reveal impaired brain development in prenatal e-cigarette exposed neonatal rats
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ABSTRACT:
PROVIDER: PRJNA769452 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16242815.fastq.gz | Fastqsanger.gz | |||
| SRR16242816.fastq.gz | Fastqsanger.gz | |||
| SRR16242817.fastq.gz | Fastqsanger.gz | |||
| SRR16242818.fastq.gz | Fastqsanger.gz | |||
| SRR16242819_1.fastq.gz | Fastqsanger.gz |
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Project description:We performed single-nucleus joint profiling of transcriptome and histone modifications, namely H3K27me3 and H3K4me1, in prenatal electronic cigarette exposed neonatal rat prefrontal cortex. We found that e-cig not only induced unique histone mark patterns for H3K27me3-H3K4me1 within the gene body in many cell type-specific marker genes, e.g., Fibcd1, Slc1a3, Apq4, and Rfx4, but also caused a differential gene expression for these genes. We demonstrated that H3K27me3-H3K4me1 bivalency regulated the neuronal lineage differentiation by controlling the accessibility of promoter regions in genes responsible for cell specifications. Prenatal e-cig exposure also caused differential gene expressions in both excitatory and inhibitory neurons in many genes involved in specific neuronal functions, which was orchestrated by different H3K27me3-H3K4me1 methylations. Furthermore, prenatal e-cig smoking altered the gene expression of circadian genes involved in circadian entrainment and circadian rhythm including calcium signaling genes Cacna1c, Camk2b, and Ryr2; cAMP and protein kinase signaling transduction gene Adcy1 and Prkcb; as well as synaptic transmitter receptor Gria4. These results suggested that nicotine addiction could be epigenetically imprinted at a very early stage of brain development. Our study showed a profound effect of epigenomic regulation of histone marks by prenatal e-cig exposure on neuronal lineage development and highlighted a new underlying epigenetic mechanism of nicotine addiction, which could potentially lead to the identification of therapeutical targets for nicotine abuse disorders.
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Project description:We studied the influence of maternal vaping on rat neonates' brain development, using single nucleus -ATAC-seq (snATAC-seq) and -RNA-seq (snRNA-seq) technologies. We found that maternal vaping distorted neuronal lineage differentiation by promoting excitatory neuron and inhibiting lateral ganglionic eminence derived inhibitory neuron differentiation. Maternal vaping also diminished microglia population in rat developing brain. Functional enrichment revealed that the distorted neuronal differentiation and reduced microglia population were associated with disrupted brain calcium homeostasis and signaling. Our findings raise the concern that maternal vaping may cause adverse long-term brain damage to the offsprings. In addition, we proposed a set of brain cell specific chromatin accessibility markers for identifying rat brain cells directly from snATAC-seq data.
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Project description:In infants, smoke exposure is associated with more respiratory illnesses and decreased lung function. We hypothesized that perinatal lung is particularly susceptible to the damaging effects of cigarette smoke (CS) and that exposure to CS during this period may alter expression of immune response genes and adversely affect lung growth. To test this, we exposed neonatal mice to 14 days of CS. Immediately after exposure to CS, pulmonary gene expression profiling was performed on 2-week-old CS-exposed lung and age-matched control lung. Nitrotyrosine, TUNEL, MAC3, and phospho-SMAD-2 (p-SMAD2) staining was also performed. At 8 weeks of age, lung volume measurements were determined and mean linear intercept measurements were calculated. Pulmonary gene expression profiling revealed that CS exposure significantly inhibited type 1 and type 2 interferon pathway genes in neonatal lung, compared with age-matched control lung. Neonatal CS-exposed lung also had a significant increase in n-tyrosine, TUNEL, and p-SMAD2 staining when compared with adult CS-exposed lung and age-matched control lung. Lung volumes at 8 weeks of age were modestly but significantly decreased in mice exposed to CS in the neonatal period compared with age-matched controls, consistent with impaired lung growth. The results of this study indicate that exposure to CS during the neonatal period inhibits expression of genes involved in innate immunity and mildly impairs postnatal lung growth. These findings may in part explain the increased incidence of respiratory symptoms in infants and children exposed to CS.
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Project description:Although emerging evidence reveals that vaping alters the function of the central nervous system, the effects of maternal vaping on offspring brain development remain elusive. Using a well-established in utero exposure model, we performed single-nucleus ATAC-seq (snATAC-seq) and RNA sequencing (snRNA-seq) on prenatally e-cigarette-exposed rat brains. We found that maternal vaping distorted neuronal lineage differentiation in the neonatal brain by promoting excitatory neurons and inhibiting lateral ganglionic eminence-derived inhibitory neuronal differentiation. Moreover, maternal vaping disrupted calcium homeostasis, induced microglia cell death, and elevated susceptibility to cerebral ischemic injury in the developing brain of offspring. Our results suggest that the aberrant calcium signaling, diminished microglial population, and impaired microglia-neuron interaction may all contribute to the underlying mechanisms by which prenatal e-cigarette exposure impairs neonatal rat brain development. Our findings raise the concern that maternal vaping may cause adverse long-term brain damage to the offspring.
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Project description:Prenatal stress (PS) could cause depression of offprsing. Here, relative quantitative phosphoproteomics of hippocampus of PS-S and CON offspring rats were performed using LC-MS/MS to confirm known pathways and identify new areas of depression. A total of 6,790 phosphopeptides, 9,817 phosphorylation sites and 2978 phosphoproteins were detected. Among the 2978 phosphoproteins, 1760 (59.09%) with more than two phosphorylated sites, ENSRNOP00000023460 protein has more than 117 phosphorylated sites, and the average distribution of modification sites per 100 amino acids was 2.97. There were 197 different phophpeptides, including 140 increased phosphopeptides and 57 decreased phosphopeptides in PS-S offspring rats when compared to the CON offspring rats. These differential phosphopeptides corresponded to 100 upregulated and 44 downregulated phosphoproteins respectively. GO enrichment analysis these different phosphoproteins in the first five enrichments of CC category, MF category and BP category were involved in a total of 35 different phosphoproteins and these phosphoproteins were mainly related to myelin, microtubule and synapse associated proteins. The first five enrichment of KEGG pathways were found to be involved in many essential biological pathways, and the first five pathways included amphetamine addiction, insulin secretion, cushing syndrome and circadian entrainment signaling pathway. And these first five pathways were related to nine proteins including Adcy9, Apc, Cacna1c, Camk2a, Camk2b, Camk2g, Ctnnd2, Grin2a, Stx1a. Further research is needed to understand the precise role of these pathways in the depressive-like behavior of offspring rats caused by PS.
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