Effects of glucose transporter expression on VSMC
Ontology highlight
ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE15713 | GEO | 2009/10/23
SECONDARY ACCESSION(S): PRJNA116605
REPOSITORIES: GEO
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Project description:Hypothesis: Overexpression of the GLUT1 facilitative glucose transporter, in A7r5 vascular smooth muscle cells, is sufficient and/or necessary to induce alterations in gene expression which influence apoptosis, growth, and proliferation. Experiment Overall Design: Scientific Approach: A7r5 rat embryonic vascular smooth muscle cells (VSMCs) (ATCC, CRL-1444) were infected for 72 hours with adenoviral vectors containing human GLUT1 or empty vector controls at a multiplicity of infection of 10 (MOI of 1 = 100 particles/cell) and grown in both high glucose (25mM) and low glucose (5.5mM) media. The human GLUT1 cDNA adenoviral vector and empty vector controls were a gift from Dr Arno Kumagai (University of Michigan). Total RNA was isolated using TRIzol (Invitrogen Life Technologies, Carlsbad, CA), followed by extraction with phenol/chloroform until the interface was clear. Total RNA was further purified using Qiagen RNeasy Mini Kit (Qiagen 74106). Immunoblot analysis was conducted to confirm GLUT1 overexpression at the time of Total RNA isolation (72 hours post-infection) for each condition. Experiment Overall Design: Number of chips: Total RNA was isolated from each of 2 conditions (control cells in low glucose (5.5mM), and GLUT1 overexpressing cells in low glucose), on three separate days and pooled to obtain one sample for each condition. In total we submitted two samples.
2009-11-07 | E-GEOD-15713 | biostudies-arrayexpress
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Project description:Vascular smooth muscle cells (VSMCs) are derived from distinct embryonic origins. Vessels originating from differing smooth muscle cell populations have distinct vascular and pathological properties of calcification, atherosclerosis, and structural defects such as aneurysm and coarctation. We hypothesized that domains within a vessel vary in phenotype based on embryonic origin. We used microarrays to detail the expression differences in vasculature of different embryonic origin. Mouse tissues were selected from different vascular compartments for RNA extraction and hybridization on Affymetrix microarrays. We sought to identify embryonic origin-specific expression profiles.
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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
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Project description:Vascular smooth muscle cells (VSMCs) are derived from distinct embryonic origins. Vessels originating from differing smooth muscle cell populations have distinct vascular and pathological properties of calcification, atherosclerosis, and structural defects such as aneurysm and coarctation. We hypothesized that domains within a vessel vary in phenotype based on embryonic origin. We used microarrays to detail the expression differences in vasculature of different embryonic origin.
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Project description:FL patients with high GLUT1 levels are at increased risk for early relapse and show only limited responses to PI3K inhibitors. The development of new therapies requires an understanding of the changes in their tumor immune microenvironment (TIME). Using novel IMC and proteomics techniques, we comprehensively identified distinguishing features in the TIME as a function of GLUT1 levels. Bioinformatics analyses identified a crosstalk between GLUT1 and TIME in tumor development and suggest that FL patients expressing high GLUT1 may benefit from metabolic-modulating therapies to prevent early relapse.
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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.
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Project description:Endothelial cells (ECs) not only form passive blood conduits. They actively contribute to nutrient transport and establish an instructive vascular niche to maintain and restore organ homeostasis. The role of the endothelium in the maintenance of muscle glucose homeostasis is however poorly understood. Here we show that, in skeletal muscle, the endothelial glucose transporter 1 (Glut1/Slc2a1) controls glucose uptake not via affecting transendothelial glucose transport, but via vascular niche control of muscle resident macrophages. Lowering endothelial glut1 via genetic depletion (glut1EC) or upon short-term high-fat diet increased angiocrine osteopontin (OPN/SPP1) secretion, promoting resident muscle macrophage activation and proliferation which impairs muscle insulin sensitivity. Consequently, co-deleting Spp1 from the endothelium prevented macrophage accumulation, reduced muscle OPN levels, and improved insulin sensitivity in glut1EC mice. Mechanistically, glut1-dependent endothelial glucose metabolic rewiring increased OPN in a serine metabolism-dependent fashion. Our data illustrate how the glycolytic endothelium creates a niche that controls resident muscle macrophage phenotype and function and directly links resident muscle macrophages to the development of muscle insulin resistance.
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Project description:Endothelial cells (ECs) not only form passive blood conduits. They actively contribute to nutrient transport and establish an instructive vascular niche to maintain and restore organ homeostasis. The role of the endothelium in the maintenance of muscle glucose homeostasis is however poorly understood. Here we show that, in skeletal muscle, the endothelial glucose transporter 1 (Glut1/Slc2a1) controls glucose uptake not via affecting transendothelial glucose transport, but via vascular niche control of muscle resident macrophages. Lowering endothelial glut1 via genetic depletion (glut1EC) or upon short-term high-fat diet increased angiocrine osteopontin (OPN/SPP1) secretion, promoting resident muscle macrophage activation and proliferation which impairs muscle insulin sensitivity. Consequently, co-deleting Spp1 from the endothelium prevented macrophage accumulation, reduced muscle OPN levels, and improved insulin sensitivity in glut1EC mice. Mechanistically, glut1-dependent endothelial glucose metabolic rewiring increased OPN in a serine metabolism-dependent fashion. Our data illustrate how the glycolytic endothelium creates a niche that controls resident muscle macrophage phenotype and function and directly links resident muscle macrophages to the development of muscle insulin resistance.
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