Single nuclei RNAseq of human fetal cardiac cells from the epicardium of 10PCW and 11PCW
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1006435 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25679703_1.fastq.gz | Fastqsanger.gz | |||
| SRR25679703_2.fastq.gz | Fastqsanger.gz | |||
| SRR25679704_1.fastq.gz | Fastqsanger.gz | |||
| SRR25679704_2.fastq.gz | Fastqsanger.gz |
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Project description:Here we characterize human fetal cardiac lymphatic vessel development and reveal a new role for cells that reside in the epicardium as a source of progenitors involved in cardiac lymphatic differentiation. The single nuclei (sn) Multiome data of the human heart reveal the plasticity and the heterogeneity of the cardiac lymphatic endothelium. We have captured nuclei from a novel population of lymphatic progenitors in the epicardium and performed an integrative snRNAseq and snATACseq analysis to define the gene expression and gene regulatory landscape of these cardiac lymphatic cells in human fetal hearts.
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Project description:The goal of this study was to perform transcriptional profiling of single epicardium-derived cells during early cardiac development. Epicardium enriched Wilms Tumor Gene 1 (Wt1) genetic lineage tracing mouse line (Wt1CreERT2/+; R26mTmG) was utilized to collect fluorescently labeled epicardial cells at embryonic day (E) 12.5 and following epicardial-to-mesenchymal transition at E16.5. Additionally, single cell transcriptional profiling was performed in endothelial cells that were collected from Wt1CreERT2/+ mice and Wt1CreERT2/+;MRTF-A-/-;MRTF-Bflox/flox to generate myocardin-related transcription factor A and B gene deletions in the epicardium and evaluate the impact of deleting a mechanosensitive gene program on coronary vasculature development at E14.5. This transcriptional data provides a resource to determine relative mRNA changes in epicardium-derived cells and endothelial cells during significant stages of cardiac development.
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Project description:Transcriptional profiling of fetal forebrain using single cell/nuclei RNAseq, bulk RNAseq and CUT&RUN
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Project description:This study is associated with the GEO accession GSE216019. Abstract from article: Re-activating quiescent adult epicardium represents a potential therapeutic approach for human cardiac regeneration. However, the exact molecular differences between inactive adult and active foetal epicardium are not known. Here, we combined foetal and adult human hearts for the first time using single-cell and single-nuclei RNA sequencing, and compared epicardial cells from both stages. We found a migratory fibroblast-like epicardial population only in the foetal heart and foetal epicardium expressed angiogenic gene programs, while the adult epicardium was solely mesothelial and immune-responsive. Furthermore, we predicted that adult hearts may still receive foetal epicardial paracrine communication, including WNT-signalling with endocardium, reinforcing the validity of regenerative strategies that administer or reactivate epicardial cells in situ. Finally, we explained graft efficacy of our human embryonic stem-cell derived epicardium model, by noting its similarity to human foetal epicardium. Overall, our study defines epicardial programs of regenerative angiogenesis absent in adult hearts, contextualises animal studies, and defines epicardial endpoints required for effective human heart regeneration.
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Project description:The HH16/17 chicken proepicardium (PE) gives rise to the embryonic epicardium (Epi) which significantly contributes formation of the coronary vasculature during cardiac development. In contrast to explanted Epi cells, explanted PE cells can undergo differentiation into a cardiac myocyte phenotype. In order to assess which genes are associated with PE differentiation into distinc cellular lineages, two interconnented microarray gene-expression series were performed. 1: Gene-expression profiles at 12, 24, 36, 48, 60, 72 and 120 hours during cardiac myocyte differentiation from including the HH16/17 PE (t0h) were determined by hybridizing Cy3 and Cy5 labelled amplified RNA to the ArkGen 20K oligo arrays in a 2-color looped experiment design, i.e., hybridization of successive time-points per array, including dye swaps, resulting in four technical replicates for each time point. 2: Gene expression changes during normal embryonic Epi maturation were assess by hybridizing Epi from stages HH25, HH29, HH32 and HH37 in all possible pair-wise combinations, including dye-swaps, leading to 6 replicates per time point. To allow for valid comparisons between the Epi and untreated PE differentiation, these two array series were connected via hybridization of both Epi stage HH25 and HH29 with the PE explant at 48 hours in culture, with dye swaps. Keywords: time course, cardiac myocyte differentiation, embryonic coronary vessel formation, cell type comparison, mRNA expression Proepicardium to cardiac myocyte differentiation: 16 arrays for 8 time points [t0h,t12h,t24h,t36h,t48h,t60h,t72h,t120h]; successive time points hybridized per array in a loop design with dye swaps + Embryonic epicardium dfferentiation: 12 arrays for 4 time points [HH25,HH29,HH32,HH37]; all possible sample combination were hybridized with dye swaps + Epicardium to Proepicardium data connection: 4 arrays; comparing HH25 and HH29 Epicardium to t48h Proepicardium with dye swaps.
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Project description:The embryonic epicardium provides a source of multipotent progenitors for cardiac lineages, including pericytes, fibroblasts and smooth muscle cells. However, it remains unclear if the epicardium comprises of heterogeneous progenitors or if epicardial cells are multipotent. Using scRNA-seq, we analysed the expression profile of epicardial and epicardial-derived cells at E15.5 and found no evidence of discrete epicardial sub-compartments. Our findings also support the notion that epicardial fate is specified after epithelial-mesenchymal transition, not pre-determined.
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Project description:Re-activating quiescent adult epicardium represents a potential therapeutic approach for human cardiac regeneration. However, the exact molecular differences between inactive adult and active foetal epicardium are not known. Here, we combined foetal and adult human hearts for the first time using single-cell and single-nuclei RNA sequencing, and compared epicardial cells from both stages. We found a migratory fibroblast-like epicardial population only in the foetal heart and foetal epicardium expressed angiogenic gene programs, while the adult epicardium was solely mesothelial and immune-responsive. Furthermore, we predicted that adult hearts may still receive foetal epicardial paracrine communication, including WNT-signalling with endocardium, reinforcing the validity of regenerative strategies that administer or reactivate epicardial cells in situ. Finally, we explained graft efficacy of our human embryonic stem-cell derived epicardium model, by noting its similarity to human foetal epicardium. Overall, our study defines epicardial programs of regenerative angiogenesis absent in adult hearts, contextualises animal studies, and defines epicardial states required for effective human heart regeneration.
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Project description:Epicardial cells can undergo epithelium-to-mesenchymal transition (EMT) upon which the epicardium-derived cells (EPDCs) migrate into the myocardium and deliver growth factors or differentiate into smooth muscle cells or fibroblasts. The cell fate of EPDCs has been proposed to be determined by the persistence of subpopulations found in the proepicardial organ, but findings regarding this epicardial heterogeneity have been inconsistent. In the human heart, the composition of the developing epicardium is largely unknown. Here we performed a direct analysis of the human fetal epicardium through single cell RNA sequencing to investigate its composition and to search for regulators of developmental processes
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Project description:Poor maternal nutrition causes intrauterine growth restriction (IUGR); however, its effects on fetal cardiac development are unclear. We have developed a baboon model of moderate maternal undernutrition, leading to IUGR. We hypothesized that the IUGR affects fetal cardiac structure and metabolism. Six control pregnant baboons ate ad-libitum (CTRL)) or 70% CTRL from 0.16 of gestation (G). Fetuses were euthanized at C-section at 0.9G under general anesthesia. Male but not female IUGR fetuses showed left ventricular fibrosis inversely correlated with birth weight. Expression of extracellular matrix protein TSP-1 was increased (p<0.05) in male IUGR. Expression of cardiac fibrotic markers TGFß, SMAD3 and ALK-1 were downregulated in male IUGRs with no difference in females. Autophagy was present in male IUGR evidenced by upregulation of ATG7 expression and lipidation LC3B. Global miRNA expression profiling revealed 56 annotated and novel cardiac miRNAs exclusively dysregulated in female IUGR, and 38 cardiac miRNAs were exclusively dysregulated in males (p<0.05). Fifteen (CTRL) and 23 (IUGR) miRNAs, were differentially expressed between males and females (p<0.05) suggesting sexual dimorphism, which can be at least partially explained by differential expression of upstream transcription factors (e.g. HNF4a, and NF?B p50). Lipidomics analysis of fetal cardiac tissue exhibited a net increase in diacylglycerol and plasmalogens and a decrease in triglycerides and phosphatidylcholines. In summary, IUGR resulting from decreased maternal nutrition is associated with sex-dependent dysregulations in cardiac structure, miRNA expression, and lipid metabolism. If these changes persist postnatally, they may program offspring for higher later life cardiac risk.
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