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Runx1+ vascular smooth muscle cells are essential for hematopoietic stem and progenitor cell development in vivo

ABSTRACT: Runx1+ vascular smooth muscle cells are essential for hematopoietic stem and progenitor cell development in vivo

PROVIDER: PRJNA956453 | ENA |

REPOSITORIES: ENA

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Runx1+ vascular smooth muscle cells are essential for hematopoietic stem and progenitor cell development in vivo

Project description:Hematopoietic stem cells (HSCs) produce all essential cellular components of the blood. Stromal cell lines supporting HSCs follow a vascular smooth muscle cell (vSMC) differentiation pathway, suggesting that some hematopoiesis-supporting cells originate from vSMC precursors. These pericyte-like precursors were recently identified in the aorta-gonad-mesonephros (AGM) region; however, their role in in vivo hematopoietic development remains unknown. Here, we identify a subpopulation of NG2+Runx1+ perivascular cells that display a sclerotome-derived vSMC transcriptomic profile. We show that deleting Runx1 in NG2+ cells impairs in vivo hematopoietic development and causes transcriptional changes in pericytes/vSMCs, endothelial cells and hematopoietic cells in the murine AGM. Importantly, this deletion leads also to a signification reduction of HSC reconstitution potential in the bone marrow in vivo. This defect is developmental, as NG2+Runx1+ cells were not detected in the adult bone marrow, demonstrating the existence of a specialised pericyte population in the HSC-generating niche, unique to the embryo.

2023-11-27 | GSE178981 | GEO

Runx1+ vascular smooth muscle cells are essential for hematopoietic stem and progenitor cell development in vivo

Project description:Runx1+ vascular smooth muscle cells are essential for hematopoietic stem and progenitor cell development in vivo

| PRJNA741787 | ENA

Runx1+ vascular smooth muscle cells are essential for hematopoietic stem and progenitor cell development in vivo

Project description:We sequenced 4 sorted cell populations: ECs, HECs, Runx1+ IAHCs and Runx1- IAHCs.

2023-11-27 | GSE229850 | GEO

Proteomic Profiling Exosomes from Vascular Smooth Muscle Cell

Project description:The components of the exosomes are essential to understand how vascular smooth muscle cells (VSMC) and endothelial cells communicate with each other. Exosomes secreted by human VSMCs were harvested and analyzed by nanoLC-MS/MS. The activity of the identified proteins were further assessed by the in vivo matrigel plug angiogenesis assay.

2018-05-07 | PXD007707 | Pride

DDX24 in Vascular Smooth Muscle Cells Is Essential for Vascular Development via Direct Association with FANCA mRNA

Project description:To investigate the role of DDX24 in vascular smooth muscle cells, RNA-seq of HASMC with DDX24 knockdown was performed.

2024-05-31 | GSE232777 | GEO

DDX24 in Vascular Smooth Muscle Cells Is Essential for Vascular Development via Direct Association with FANCA mRNA

Project description:DDX24 in Vascular Smooth Muscle Cells Is Essential for Vascular Development via Direct Association with FANCA mRNA

| PRJNA973949 | ENA

LncVSM (AK098656) down-regulation in Vascular Smooth Muscle cells

Project description:The full length of LncVSM transfected into Vascular Smooth Muscle cells to down-regulation for screening differential expression prolifes of LncVSM effecting.The empty vector transfected Vascular Smooth Muscle cells as controls. Eight Samples analyzed.

2016-01-12 | E-GEOD-76720 | biostudies-arrayexpress

LncVSM (AK098656) up/down-regulation in Vascular Smooth Muscle cells

Project description:Long non-coding RNAs (LncRNAs) in hypertensives and their mechanisms in regulating blood pressure still remain unexplored. The aim of present study is to construct the profiles of LncRNAs in blood of patients with essential hypertension and healthy controls. Methods and results, LncRNA microarray identified up-regulated, anddown-regulated LncRNAs, in hypertensives compared to their healthy controls. Among them, one vascular smooth muscle (VSM)-specific LncRNA AK096656 (LncVSM) was quantitated in plasma of patients with hypertension and their healthy controls using the real-time qRT-PCR. LncVSM shows specific expression in human arterial vascular smooth muscle cells (HASMCs) and promote its proliferation and migration. Expression profiles and Ingenuity Pathway Analysis (IPA) revealed that LncVSM activated Renin-Angiotensin Signaling (RAS). the overexpression of LncVSM would result hypertension related complications. LncVSM (AK098656) transfection

2015-12-12 | E-GEOD-75940 | biostudies-arrayexpress

To examine vascular smooth muscle cells (VSMC) under four conditions

Project description:Vascular calcification is a hallmark of atherosclerosis and end-stage renal disease (ESRD). However, the molecular mechanism of vascular calcification is poorly understood. Diabetes mellitus is increasingly recognized as the most important cause for atherosclerosis and ESRD. Emerging evidence supports the concept that vascular calcification resembles the process of osteogenesis, in which the vascular smooth muscle cells (VSMC) undergo osteochondrogenic differentiation. Recently, we have established an in vitro calcification system with primary mouse VSMC. With the use of osteogenic stimuli, we induced trans-differentiation of primary mouse VSMC into bone-like cells. Interestingly stroptozotocin (STZ), O-GlcNAcase inhibitor and a drug that has been used to induce diabetes in mice, was able to induce calcification of VSMC and the expression of the osteogenic transcription factor Runx2, suggesting glycosylation may be involved in regulation of Runx2. We have reported an essential role of Runx2 in oxidative stress-induce VSMC calcification and have recently generated a tissue specific mouse with Runx2 ablation in smooth muscle cells. Therefore, we will use STZ and other relevant reagents in the glucose synthesis/metabolism pathways as stimuli for VSMC calcification to characterize the glycogene profiles during VSMC calcification. Results from VSMC of Runx2 knockout mice will be compared with those from control mice to determine the regulation of calcification-associated glycogenes by Runx2 in response to STZ. These studies will provide foundation for further mechanistic studies and may lead to identification of novel strategies and targets for diabetes-induced vascular calcification. To examine vascular smooth muscle cells (VSMC) under two conditions: 1) wild-type VSMC differentiated into bone-like cells with osteogenic media, 2) wild-type VSMC treated with STZ and osteogenic media

2011-09-05 | E-GEOD-31928 | biostudies-arrayexpress

YAP/TAZ in vascular smooth muscle

Project description:YAP/TAZ in vascular smooth muscle

| PRJNA610067 | ENA