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Transcriptional dynamics in HUVECs and fetal endothelial progenitor cells during establishment of innate immune memory

ABSTRACT: Transcriptional dynamics in HUVECs and fetal endothelial progenitor cells during establishment of innate immune memory

PROVIDER: PRJNA749872 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15254200_1.fastq.gz	Fastqsanger.gz
	SRR15254200_2.fastq.gz	Fastqsanger.gz
	SRR15254201_1.fastq.gz	Fastqsanger.gz
	SRR15254201_2.fastq.gz	Fastqsanger.gz
	SRR15254202_1.fastq.gz	Fastqsanger.gz

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Transcriptional dynamics in HUVECs and fetal endothelial progenitor cells during establishment of innate immune memory

Project description:Innate immune memory (also known as Trained immunity) is a phenomenon whereby innate immune cells such as monocytes or macrophages undergo functional reprogramming after exposure to certain microbial components, altering their responses to future exposures. Recent data show that this phenomenon occurs in endothelial cells. In this study we mapped the transcriptional changes that occur in two different types of fetal endothelial cells in response to an initial viral ligand, followed by a secondary bacterial exposure.

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GATA2 restricts genomic actions of innate immune mediators on fetal hematopoietic progenitor cells

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GATA2 restricts genomic actions of innate immune mediators on fetal hematopoietic progenitor cells

Project description:GATA2 restricts genomic actions of innate immune mediators on fetal hematopoietic progenitor cells

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Project description:HS-induced proteome changes in WT and DNAJA1-KO cells were quantified using label free-based quantitative proteomic analysis. Four groups:wild type HUVECs group, DNAJA1 knockout HUVECs group, WT HUVECs with heat stress group, DNAJA1 knockout HUVECs with heat stress group,were conducted label free-based quantitative proteomic analysis to detect the mechanism of DNAJA1's protective effects on heat stress.

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Single-cell deciphering of human fetal innate lymphoid cell development

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Sexual Dimorphism of Preeclampsia-Dysregulated Transcriptomic Profiles and Endothelial Function in Fetal Endothelial Cells

Project description:Preeclampsia-offspring have increased risks of developing cardiovascular disorders in adulthood, implicating that preeclampsia programs fetal vasculature in utero. Fetal sex is associated with the risk of preeclampsia but the underlying mechanisms are unclear. We hypothesize that preeclampsia alters fetal endothelial gene expression and disturbs cytokines and growth factors-induced endothelial function in a fetal sex-specific manner. Methods: RNAseq analysis was performed with female and male unpassaged (P0) human umbilical vein endothelial cells (HUVECs) from normotensive and preeclamptic (PE) pregnancies and verified by RT-qPCR. Results: PE dysregulate 926 and 172 genes in female and male P0-HUVECs, respectively. PE differentially dysregulates cardiovascular diseases (i.e. heart failure) and endothelial function (i.e. endothelial cell migration, calcium, eNOS, and iNOS signaling)-associated genes in female and male P0-HUVECs. PE also differentially dysregulates TNF-, TGFβ1-, FGF2-, and VEGFA-regulated gene networks in female and male P0-HUVECs. Conclusions: There are sexual dimorphisms of PE-dysregulated cardiovascular diseases and endothelial function-associated genes/pathways in fetal endothelial cells in association with sexual dimorphisms of PE-dysregulated fetal endothelial function.

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Project description:Memory CD8+ T cells have the ability to provide lifelong immunity against pathogens. Although memory features generally arise after challenge with a foreign antigen, naïve CD8 single positive (SP) thymocytes may acquire phenotypic and functional characteristics of memory cells in response to cytokines such as interleukin-4. This process is associated with the induction of the T-box transcription factor Eomesodermin (EOMES). However, the underlying molecular mechanisms remain ill-defined. Using epigenomic profiling, we show that these innate memory CD8SP cells acquire only a portion of the active enhancer repertoire of conventional memory cells. This reprograming is secondary to EOMES recruitment, mostly to RUNX3-bound enhancers. Furthermore, EOMES is found within chromatin-associated complexes containing BRG1 and promotes the recruitment of this chromatin remodelling factor. Also, the in vivo acquisition of EOMES-dependent program is BRG1-dependent. In conclusion, our results support a strong epigenetic basis for the EOMES-driven establishment of CD8+ T cell innate memory program.

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Single-cell deciphering of human fetal innate lymphoid cell development

Project description:The functions of innate lymphoid cells (ILCs) in immune system are increasingly appreciated, whereas the early development of ILCs in human remains elusive. In this study, we sorted humanhematopoietic stem progenitor cells, lymphoid progenitors, presumed ILC progenitor/precursors and mature ILCs in the fetal hematopoietic, lymphoid and non-lymphoid tissues, from 8 to 12 PCW,for single-cell RNA-sequencing, followed by computational analysis and functional validation. We delineated the early phase of ILC development, from hematopoietic stem progenitor cells to multipotent lymphoid progenitors and to ILC progenitors, which mainly occurred in fetal liver and intestine. We further unveiled interleukin-3 receptor alpha (IL-3RA) as the surface marker for the lymphoid progenitors with T cell, B cell and ILC potentials. Notably, we determined the heterogeneity and tissue distribution of each ILC subpopulation, revealing the shared proliferating characteristics of the precursors of each ILC subtype. Additionally, a novel unconventional ILC2 subpopulation (CRTH2-CCR9+ ILC2) was identified in fetal thymus. Taken together, our study illuminates the precise cellular and molecular features underlying the stepwise formation of human fetal ILC hierarchy with remarkable spatiotemporal heterogeneity.

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