Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Stress-induced RNA–chromatin interactions promote endothelial dysfunction (scRNA-seq human vascular)

ABSTRACT: Stress-induced RNA–chromatin interactions promote endothelial dysfunction (scRNA-seq human vascular)

PROVIDER: PRJNA657567 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12462567_1.fastq.gz	Fastqsanger.gz
	SRR12462567_2.fastq.gz	Fastqsanger.gz
	SRR12462568_1.fastq.gz	Fastqsanger.gz
	SRR12462568_2.fastq.gz	Fastqsanger.gz
	SRR12462569_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 20

Similar Datasets

Stress-induced RNA–chromatin interactions promote endothelial dysfunction

Project description:Stress-induced RNA–chromatin interactions promote endothelial dysfunction

| PRJNA558554 | ENA

Stress-induced RNA–chromatin interactions promote endothelial dysfunction (iMARGI)

Project description:Stress-induced RNA–chromatin interactions promote endothelial dysfunction (iMARGI)

| PRJNA558556 | ENA

Stress-induced RNA–chromatin interactions promote endothelial dysfunction (Hi-C)

Project description:Stress-induced RNA–chromatin interactions promote endothelial dysfunction (Hi-C)

| PRJNA558553 | ENA

Stress-induced RNA–chromatin interactions promote endothelial dysfunction (scRNA-seq)

Project description:Stress-induced RNA–chromatin interactions promote endothelial dysfunction (scRNA-seq)

| PRJNA558555 | ENA

Stress-induced RNA–chromatin interactions promote endothelial dysfunction (RNA-seq)

Project description:Stress-induced RNA–chromatin interactions promote endothelial dysfunction (RNA-seq)

| PRJNA657560 | ENA

Stress-induced RNA–chromatin interactions promote endothelial dysfunction (scRNA-seq human vascular)

Project description:Chromatin-associated RNA (caRNA) has been proposed as a type of epigenomic modifier. Here, we test whether environmental stress can induce cellular dysfunction through modulating RNA-chromatin interactions. We induce endothelial cell (EC) dysfunction with high glucose and TNFα (H + T), that mimic the common stress in diabetes mellitus. We characterize the H + T-induced changes in gene expression by single cell (sc)RNA-seq, DNA interactions by Hi-C, and RNA-chromatin interactions by iMARGI. H + T induce inter-chromosomal RNA-chromatin interactions, particularly among the super enhancers. To test the causal relationship between H + T-induced RNA-chromatin interactions and the expression of EC dysfunction-related genes, we suppress the LINC00607 RNA. This suppression attenuates the expression of SERPINE1, a critical pro-inflammatory and pro-fibrotic gene. Furthermore, the changes of the co-expression gene network between diabetic and healthy donor-derived ECs corroborate the H + T-induced RNA-chromatin interactions. Taken together, caRNA-mediated dysregulation of gene expression modulates EC dysfunction, a crucial mechanism underlying numerous diseases.

2020-08-17 | GSE156341 | GEO

Stress-induced RNA–chromatin interactions promote endothelial dysfunction (iMARGI replicate 2)

Project description:Stress-induced RNA–chromatin interactions promote endothelial dysfunction (iMARGI replicate 2)

| PRJNA657559 | ENA

Stress-induced RNA–chromatin interactions promote endothelial dysfunction (iMARGI)

2020-08-17 | GSE135355 | GEO

Multiomics Profiling of Extracellular Vesicles Supports Their Involvement in Endothelial Senescence-Associated Vascular Dysfunction

Project description:Dysfunction of vascular endothelium is characteristic of many aging-related diseases, including Alzheimers disease (AD) and AD-related dementias (ADRD). While it is widely posited that endothelial cell dysfunction contributes to the pathogenesis and/or progression of AD/ADRD, it is not clear how. A plausible hypothesis is that intercellular trafficking of extracellular vesicles (EVs) from senescent vascular endothelial cells promotes vascular endothelial cell dysfunction. To test this hypothesis, we compared the expression of proteins and miRNAs in EVs isolated from early passage (EP) vs. senescent (SEN) primary human coronary artery endothelial cells (HCAECs) from the same donor. Proteomics and miRNA libraries constructed from these EV isolates were evaluated using FunRich gene ontology analysis to compare functional enrichment between EP and SEN endothelial cell EVs (ECEVs). Replicative senescence was associated with altered EV abundance and contents independent of changes in EV size. Unique sets of miRNAs and proteins were differentially expressed in SEN-ECEVs, including molecules related to cell adhesion, barrier integrity, receptor signaling, endothelial-mesenchymal transition and cell senescence. miR-181a-5p was the most upregulated miRNA in SEN-ECEVs, increasing >5-fold. SEN-ECEV proteomes supported involvement in several pro-inflammatory pathways consistent with senescence and the senescence-associated secretory phenotype (SASP). These data indicate that SEN-ECEVs are enriched in bioactive molecules implicated in senescence-associated vascular dysfunction, blood-brain barrier impairment, and AD/ADRD pathology. These observations suggest involvement of SEN-ECEVs in the pathogenesis of vascular dysfunction associated with AD/ADRD.

2024-08-23 | MSV000095687 | MassIVE

Stress-induced RNA–chromatin interactions promote endothelial dysfunction (RNA-seq)

2020-08-17 | GSE156340 | GEO