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Loss of Jagged1 in mature endothelial cells causes vascular dysfunction with alterations in smooth muscle phenotypes

ABSTRACT: Loss of Jagged1 in mature endothelial cells causes vascular dysfunction with alterations in smooth muscle phenotypes

PROVIDER: PRJNA862173 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20636057_1.fastq.gz	Fastqsanger.gz
	SRR20636057_2.fastq.gz	Fastqsanger.gz
	SRR20636059_1.fastq.gz	Fastqsanger.gz
	SRR20636059_2.fastq.gz	Fastqsanger.gz
	SRR20636061_1.fastq.gz	Fastqsanger.gz

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Loss of Jagged1 in mature endothelial cells causes vascular dysfunction with alterations in smooth muscle phenotypes

Project description:Notch signaling is an evolutionarily conserved pathway that functions via direct cell-cell contact. The Notch ligand Jagged1 (Jag1) has been extensively studied in vascular development, particularly for its role in smooth muscle cell maturation. Endothelial cell-expressed Jag1 is essential for blood vessel formation by signaling to nascent vascular smooth muscle cells and promoting their differentiation. Given the established importance of Jag1 in endothelial cell/smooth muscle crosstalk during development, we sought to determine the extent of this communication in the adult vasculature for blood vessel function and homeostasis.

2022-08-01 | GSE209736 | GEO

Single-cell RNA-seq Reveals Unique Vascular Smooth Muscle Cell Phenotypes in Culture

Project description:Background. Heterogeneity in vascular smooth muscle cells (VSMCs) has been classically defined with a small set of predefined markers. Single cell genomics provides a unique unbiased approach to evaluate VSMC phenotypes. Objectives. The goal of this study was to define the heterogeneity of primary murine VSMCs grown in culture. VSMCs grown in culture are routinely used as a model of VSMCs in the vessel wall. We wanted to better understand the assumptions of this model. RNA sequencing was performed on single aortic VSMCs from 3-4 month old male mice at passages 1 and 2 (P1 and P2). Single cell contractility measurements were performed using Traction Force microscopy.

2016-03-22 | E-GEOD-79436 | biostudies-arrayexpress

Single-cell RNA-seq Reveals Unique Vascular Smooth Muscle Cell Phenotypes in Culture

2016-03-22 | GSE79436 | GEO

Jagged1 regulates miRNA expression profile

Project description:miRNA expression profiles of HMECs treated with 40mM Jagged1 (JAG1) or the control peptide for 1 day Genome-wide miRNA PCR array analysis was performed using human miRNA PCR arrays (MIHS216Z, SABiosceinces) acccording to the manufacturer's instructions

2014-05-30 | E-GEOD-56801 | biostudies-arrayexpress

Tumor-derived Jagged1- and Notch-dependent transcription changes in MC3T3-E1 osteoblasts

Project description:Transcriptional profiling of MC3T3-E1 osteoblasts that were flow cytometry-separated from cocultures with control or Jagged1-overexpressing tumor cells and treated with either DMSO control or 1μM MRK-003 (gamma-secretase inhibitor). One cell line (MC3T3-E1) cells: four different experimental conditions: cultured with (1) control tumor cells + DMSO; (2) Jagged1-overexpressing tumor cells + DMSO; (3) control tumor cells + MRK-003; (4) Jagged1-overexpressing tumor cells + MRK-003. Each experiment has two biological replicates. Total, 8 samples.

2010-08-15 | E-GEOD-20517 | biostudies-arrayexpress

Jagged1 regulates miRNA expression profile

Project description:miRNA expression profiles of HMECs treated with 40mM Jagged1 (JAG1) or the control peptide for 1 day

2014-05-30 | GSE56801 | GEO

Differential gene expression in Jagged1 treated human dental pulp cells.

Project description:The present study aimed to determine mRNA expression profilling of indirect immobilized Jagged1 treated human dental pulp cells. Human dental pulp cells were seeded on indirect immobilized Jagged1 surface for 24 h. Cells on hFc immobilized surface was employed as the control. RNA sequencing was performed using NextSeq500, Illumina. Data were processed on FastQC and FastQ Toolkit and subsequently mapped with Homo sapiens hg38 using TopHat2. Mapped data were processed through Cufflink2 and Cuffdiff2. Results demonstrated 1,465 differentially expressed genes in Jagged1 treated cells compared with the control. Enriched pathway analysis revealed that Jagged1 treated cells upregulated genes mainly involved in extracellular matrix organization, disease, and signal transduction categories. However, genes related to cell cycle, DNA replication and DNA repair categories were downregulated. In conclusion, Jagged1 activates Notch signaling and regulates cell cycle pathway in hDPs.

2017-04-04 | GSE94989 | GEO

Genes regulated/modulated by jagged1 in endothelial cells during inflammation

Project description:Proinflammatory activation of endothelial cells leads to recruitment of leukocytes by upregulation of adhesion molecules and presentation of chemoattractants. In response to such activation there is also a strong shift in the endothelial expression of Notch ligands, with downregulation of Dll4 and a upregulation of JAG1. To assess whether Jagged1 would affect the endothelial activation profile, we suppressed JAG1 expression during IL-1β-induced activation by means of siRNA and performed a genome-wide transcriptome analysis. Our results show for the first time that Jagged1 modulates the transcription profile of activated endothelial cells and describe data that imply a role for Jagged1 in sharpening the inflammatory profile of the vasculature, giving it an edge towards leukocyte recruitment. These findings imply that Jagged1 might be a potential therapeutic target to attenuate inflammation and reduce tissue damage in inflammatory diseases.

2018-08-29 | GSE39180 | GEO

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Project description:The prevalence of cardiovascular disease varies with sex, and the impact of intrinsic sex-based differences on vasculature is not well understood. Animal models can provide important insight into some aspects of human biology, however not all discoveries in animal systems translate well to humans. To explore the impact of chromosomal sex on proteomic phenotypes, we used iPSC-derived vascular smooth muscle cells from healthy donors of both sexes to identify sex-based proteomic differences and their possible effects on cardiovascular pathophysiology. Our analysis confirmed that differentiated cells have a proteomic profile more similar to healthy primary aortic smooth muscle than iPSCs. We also identified sex-based differences in iPSC-derived vascular smooth muscle in pathways related to ATP binding, glycogen metabolic process, and cadherin binding as well as multiple proteins relevant to cardiovascular pathophysiology and disease. Additionally, we explored the role of autosomal and sex chromosomes in protein regulation, identifying that proteins on autosomal chromosomes also show sex-based regulation that may affect the protein expression of proteins from autosomal chromosomes. This work supports the biological relevance of iPSC-derived vascular smooth muscle cells as a model for disease, and further exploration of the pathways identified here can lead to the discovery of sex-specific pharmacological targets for cardiovascular disease.

2024-07-23 | MSV000095417 | MassIVE

Vascular smooth muscle selective deletion of Srf

Project description:Previous efforts to conditionally delete the Srf transcription factor in smooth muscle lineages were met with early demise of the mouse due to a gastrointestinal (GI) obstruction phenotype. We have developed a new, more VSMC selective Cre recombinase mouse (Itga8-CreERT2), that circumvents the GI phenotype thus affording the opportunity to evaluate, in an unambiguous manner, VSMC phenotypes where Srf is reduced. The mice live for at least 6 months post-tamoxifen and here we report the first RNA-seq experiments in mouse aortic SMC where Srf is reduced.

2020-04-18 | GSE138824 | GEO

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