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Whole transcriptome analysis of mouse aortas and kidneys with or without deletion of the EGFR in endothelial cells after 18 weeks of high fat diet

ABSTRACT: Vascular EGF receptors (EGFR) are supposed to be relevant for function and structure of arterial vessels. Recently, we showed in genetic mouse models that vascular smooth muscle (VSMC) EGFR is required for proper physiological function and structure as well as for pathophysiological alterations induced by angiotensin II or obesity. The importance of endothelial (EC) EGFR in vivo is unknown. Therefore we analyzed the impact of EC-EGFR knockout on vascular and renal function under control condition as well as in obesity in comparison to VSMC-KO.

ORGANISM(S): Mus musculus

PROVIDER: GSE158197 | GEO | 2021/04/01

REPOSITORIES: GEO

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Whole transcriptome analysis of mouse aortas and kidneys with or without deletion of the EGFR in vascular smooth muscle cells after 18 weeks of high fat diet

Project description:Obesity causes diabetes type 2 (DMT2) leading to vascular dysfunction and finally renal end-organ damage. Vascular smooth muscle (VSM) EGF receptor (EGFR) modulates vascular wall homeostasis in part via serum response factor (SRF), a major regulator of VSM differentiation and a sensor for glucose. We investigated the role of VSM-EGFR during obesity-induced renovascular dysfunction and the EGFR-hyperglycemia crosstalk.

2020-03-01 | GSE144838 | GEO

Factor VII activating protease (FSAP) regulates the expression of inflammatory genes in vascular smooth muscle and endothelial cells.

Project description:Vascular smooth muscle cells (VSMC) and endothelial cells (EC) were stimulated with factor VII activating protease and transcriptional changes were determined.

2017-10-13 | E-MTAB-5592 | biostudies-arrayexpress

Transcription profiling of human umbilical vein endothelial cells (HUVEC) cultured under retroviral transduction, on different culture substrates and in different geometries

Project description:Overexpression of a caspase-resistant form of Bcl-2 (D34A) in human umbilical vein endothelial cells (EC) implanted into immunodeficient mice promotes the maturation of human EC-lined microvessels invested by vascular smooth muscle cells (VSMC) of mouse origin. In contrast, EC implants not overexpressing Bcl-2 form only simple, uncoated EC tubes. Here we compare the phenotypes of vessels formed in vivo and the transcriptomes in vitro of EC expressing different forms of Bcl-2. Wild type Bcl-2, like the caspase resistant D34A Bcl-2 mutant, is anti-apoptotic in vitro and promotes VSMC recruitment in vivo, whereas a G145E mutant that has diminished anti-apoptotic activity in vitro does not promote vessel maturation in vivo. The D34A and wild type forms of Bcl-2, but not the G145E mutant form of Bcl-2 significantly regulate RNA transcripts previously associated with EC-VSMC interactions and VSMC biology, including matrix Gla protein, insulin like growth factor binding protein (IGFBP)-2, matrix metaloproteinase-14 (MMP14), ADAM17 and Stanniocalcin-1. These effects of Bcl-2 on the transcriptome are detected in EC cultured as angiogenic 3-D tubes but are attenuated in EC cultured as 2-D monolayers. Bcl-2-regulated transcription in EC may contribute to vascular maturation, and support design of tissue engineering strategies using EC. Experiment Overall Design: This study consists of the analysis of human umbilical vein endothelial cells (HUVEC) cultured under several conditions, including retroviral transduction, as well as on different culture substrates and in different geometries. For a full description please see our paper in the journal Endothelium, 2008. For

2008-04-06 | E-GEOD-10710 | biostudies-arrayexpress

Single-Cell Transcriptomic Heterogeneity Between Conduit and Resistance Rat Mesenteric Arteries

Project description:The vascular endothelium contains morphologically similar cells throughout, but individual cells along the length of a single vascular tree or in different regional circulations function quite dissimilarly. When observations made in large arteries are extrapolated to explain the function of endothelial cells (EC) in the resistance vasculature/microcirculation, only a fraction of these observations are consistent between artery sizes. To what extent endothelial (EC) and vascular smooth muscle (VSMC) cells from different arteriolar segments of the same tissue differ phenotypically at the single-cell level remains unknown. Therefore, single-cell RNA-seq (10x Genomics) was performed using a 10X Genomics Chromium system.

2023-03-09 | GSE202244 | GEO

Bcl2-induced vascular maturation

Project description:Overexpression of a caspase-resistant form of Bcl-2 (D34A) in human umbilical vein endothelial cells (EC) implanted into immunodeficient mice promotes the maturation of human EC-lined microvessels invested by vascular smooth muscle cells (VSMC) of mouse origin. In contrast, EC implants not overexpressing Bcl-2 form only simple, uncoated EC tubes. Here we compare the phenotypes of vessels formed in vivo and the transcriptomes in vitro of EC expressing different forms of Bcl-2. Wild type Bcl-2, like the caspase resistant D34A Bcl-2 mutant, is anti-apoptotic in vitro and promotes VSMC recruitment in vivo, whereas a G145E mutant that has diminished anti-apoptotic activity in vitro does not promote vessel maturation in vivo. The D34A and wild type forms of Bcl-2, but not the G145E mutant form of Bcl-2 significantly regulate RNA transcripts previously associated with EC-VSMC interactions and VSMC biology, including matrix Gla protein, insulin like growth factor binding protein (IGFBP)-2, matrix metaloproteinase-14 (MMP14), ADAM17 and Stanniocalcin-1. These effects of Bcl-2 on the transcriptome are detected in EC cultured as angiogenic 3-D tubes but are attenuated in EC cultured as 2-D monolayers. Bcl-2-regulated transcription in EC may contribute to vascular maturation, and support design of tissue engineering strategies using EC. Keywords: genetic modification, growth condition modification.

2008-03-05 | GSE10710 | GEO

Differential Effects of TiO2 Nanotubes on Vascular Cells

Project description:The response of primary human endothelial (ECs) and vascular smooth muscle cells (VSMCs) to TiO2 nanotube arrays is studied through gene expression analysis. Microarrays revealed that nanotubes enhanced EC proliferation and motility, decreased VSMC proliferation, and decreased expression of molecules involved in inflammation and coagulation in both cell types. Network generated from significantly affected genes suggests that cells may be sensing nanotopographical cues via pathways previously implicated in sensing shear stress. DNA microarrays were used to analyze the response of primary human endothelial (ECs) and vascular smooth muscle cells (VSMCs) to nanotopographical TiO2 surfaces. The experiment incorporated a 1 color design and used Agilent arrays that contained roughly 44,00 60mer probes that provide complete coverage of the human genome. 19 arrays were hybridized and represent 4 biological replicates for each group ( with the exception of group VSMC-NT30, which has 3 biological replicates). Data was analyzed separately for each cell type ( EC or VSMC). Gene expression comparisons were made between control cells grown on flat titanium (Ti) and cells grown on either 30nm nanotubes (NT30) or 100nm nantubes ( NT-100).

2010-08-14 | E-GEOD-17676 | biostudies-arrayexpress

Active repression of Sox9 by Jag1 is required for silencing the default chondrogenic fate of the vascular smooth muscle wall [set 2]

Project description:Acquisition and maintenance of vascular smooth muscle fate is essential for the morphogenesis and function of the circulatory system. Loss of contractile properties or changes in the identity of vascular smooth muscle cells (vSMC) can result in structural alterations associated with aneurysms and vascular wall calcifications. Here we report that maturation of sclerotome-derived vSMC is dependent on a transcriptional switch between mouse embryonic days 13 and 14.5. At this time point, Jag1-mediated repression of sclerotome transcription factors Pax1, scleraxis and Sox9 is necessary to fully enable vSMC maturation. Specifically, Notch signaling in vSMC antagonizes sclerotome and cartilage transcription factors, and promotes upregulation of contractile genes. In the absence of Jag1, vSMC acquire a chondrocytic transcriptional repertoire that can lead to ossification of the vascular wall. Importantly, our findings suggest that sustained Notch signaling is essential throughout vSMC life to maintain contractile function, prevent vSMC reprogramming and promote vascular wall integrity.

2015-03-23 | GSE60642 | GEO

Active repression of Sox9 by Jag1 is required for silencing the default chondrogenic fate of the vascular smooth muscle wall [set 1]

2015-03-23 | GSE60641 | GEO

Novel Roles of Nrf3-Trim5 Axis in Vascular Smooth Muscle Cell Dysfunctions and Neointimal Hyperplasia

Project description:Neointimal hyperplasia (NIH), driven by vascular smooth muscle cell (VSMC) dysfunction, is a key factor in vascular diseases like atherosclerosis and restenosis. While Nrf3 is known to regulate VSMC differentiation, its role in NIH remains unclear. Using transcriptomic data, Nrf3 knockout mice (global), we assessed Nrf3’s impact on VSMC function and NIH. We identified Trim5, a gene linked to coronary artery disease, as a downstream target of Nrf3, which promotes autophagy in VSMCs and injured arteries, enhancing VSMC dysfunction and NIH. Nrf3 overexpression increased VSMC proliferation, migration, and inflammation, while deletion or knockdown had the opposite effects. Nrf3-/- and Nrf3ΔSMC mice showed reduced VSMC accumulation and attenuated NIH after vascular injury. These findings highlight Nrf3 as a novel modulator of VSMC dysfunction and injury-induced NIH, with potential for therapeutic targeting of the Nrf3-Trim5 axis to treat NIH-related vascular diseases.

2024-12-02 | GSE281869 | GEO

Vascular smooth muscle cell derived from iPS cell of Moyamoya disease - Comparative characterization with endothelial cell transcriptome

Project description:Transcriptome analysis of vascular smooth muscle cells differentiated from iPS-derived neural crest stem cells in Moyamoya disease Moyamoya disease (MMD) is a rare cerebrovascular disorder characterized by steno-occlusive changes in the cerebral arteries at the base of the brain with unknown etiology, although histopathological features have demonstrated as fibrocellular thickening of the intima and medial thinning on the steno-occlusive arteries. However, the pathophysiology of proliferating cells in the thickened intima is still obscure. Furthermore, biological features of the vascular smooth muscle cells are unclear in MMD. Here, we aimed to analyze whole genome gene expression profile in VSMC using induced pluripotent stem (iPS) cell line. We generated iPS cell line from the blood of MMD with RNF213 R4810K risk allele (rs112735431) or healthy control without the risk allele. VSMCs were differentiated from iPS-derived neural crest stem cells. As a result, we successfully established cranio-cervical region specific VSMC confirmed by immunocytochemistry. Biological cellular features, including cellular proliferation, migration, and contraction ability were similar in VSMCs between MMD and control. Genome-wide gene expression analysis showed similar transcriptome profile in the VSMCs between MMD and control. Differential gene expression analysis in MMD-VSMC revealed 6 differentially expressed genes (4 upregulated, 2 down regulated in MMD), including decorin (DCN, upregulated in MMD), playing an inhibitory role in angiogenesis. In conclusion, VSMCs are not impaired in cellular function with similar transcriptome profile in MMD compared to healthy control. Since many previous studies have shown impaired EC features in MMD, our study suggests EC may play more role in the vascular pathogenesis in MMD rather than VSMC.

2020-09-11 | GSE131293 | GEO

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