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Analysis of the global gene expression in VEGF-B transgenic rat hearts

ABSTRACT: We show that an excess of VEGF-B protects the heart via adaptive cardiac hypertrophy and increased coronary arterial reserve, and by inducing a shift from lipid to glucose metabolism.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE38454 | GEO | 2013/11/30

SECONDARY ACCESSION(S): PRJNA167973

REPOSITORIES: GEO

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Analysis of the global gene expression in VEGF-B transgenic rat hearts

Project description:We show that an excess of VEGF-B protects the heart via adaptive cardiac hypertrophy and increased coronary arterial reserve, and by inducing a shift from lipid to glucose metabolism. Six VEGF-B overexpressing transgenic hearts were compared to six littermate wildtype controls

2013-11-30 | E-GEOD-38454 | biostudies-arrayexpress

Analysis of the global gene expression in the rat hearts transduced with adeno-associated viral vectors coding VEGF-B

2013-11-30 | GSE38455 | GEO

Analysis of the global gene expression in the rat hearts transduced with adeno-associated viral vectors coding VEGF-B

Project description:We show that an excess of VEGF-B protects the heart via adaptive cardiac hypertrophy and increased coronary arterial reserve, and by inducing a shift from lipid to glucose metabolism. Six hearts transduced with AAV-VEGF-B were compared to six AAV-HSA (human serum albumin) controls

2013-11-30 | E-GEOD-38455 | biostudies-arrayexpress

Single cell changes in postnatal P7 and in adult cardiac endothelium upon VEGF-B overexpression

Project description:We have previously reported that mice expressing a cardiomyocyte-specific αMHC-VEGF-B transgene in the heart show a clear expansion of the coronary vasculature and cardiac hypertrophy, without significant changes in heart function. As a therapeutic way of administrating VEGF-B protective effects, we show that AAV-VEGF-B induces the proliferation of endothelial cells (EC). All the samples were analyzed using the Chromium Single-cell 3'RNA-sequencing system.

2022-03-15 | GSE128509 | GEO

Contribution of VEGF-B-induced endocardial endothelial cell lineage in physiological versus pathological cardiac hypertrophy.

Project description:ScRNA-seq was used to investigate the effects of autocrine versus paracrine VEGF-B signaling in the heart using transgenic mouse models. The paracrine model was further investigated in pregnancy-induced cardiac hypertrophy as well as in mice with ligation of the left anterior descending (LAD) coronary artery.

2024-04-19 | GSE261561 | GEO

The effects of AAV-VEGF-B and deletion of endothelial VEGFR1 on heart transcriptome in adult mice

Project description:We evaluated the effects of vascular endothelial growth factor -B (VEGF-B) and the deletion of its receptor VEGFR1 from endothelial cells on cardiac hypertrophy. Whole-genome transcriptomic analysis showed that overexpression of the ligand had similar effects on the heart transcriptome as deletion of its receptor. Both treatments also induced angiogenesis and mild cardiac hypertrophy. The aim of the study was to identify pathways, which mediate angiogenesis-induced cardiac hypertrophy.

2018-12-31 | GSE110532 | GEO

VEGF overexpressed mesoangioblasts enhance urethral and vaginal recovery following simulated vaginal birth in rats

Project description:Background: Vaginal birth causes injury to the pelvic floor and may lead to urinary incontinence. Cell therapy has been proposed to assist in functional recovery. Objective: To assess if intra-arterial injection of mesoangioblasts (MABs) or Vascular Endothelial Growth Factor (VEGF)-overexpressed MABs, improves urethral and vaginal function recovery after simulated vaginal delivery (SVD). Results: All stem-cell injected rats had external urethral sphincteric and vaginal function recovery within 14d, as compared to half of controls. Functional recovery was paralleled by improved muscle regeneration and microvascularization. Recovery was not different between autologous and allogenic MABs. MABsallo-VEGF accelerated functional recovery and increased GAP-43 expression at 7d. We detected early on in the recovery major transcriptional changes in both MABsallo and MABsallo-VEGF. MABSallo upregulated transcripts that encode proteins involved in myogenesis and dendrite development, and downregulated pro-inflammatory processes MABsallo-VEGF upregulated transcripts that encode proteins involved neuron and dendrite development and downregulates genes involved in hypoxia and oxidative stress. 7d after injury, Later MABsallo-VEGF showed a decrease in oxidative and inflammatory response compared to MABSallo treated urethras. These pathways are also downregulated in animals that have recovered at 7d, compared to non-recovered animals. Conclusion: Intra-arterial injection of MABsallo-VEGF enhances neuroregeneration and accelerates functional urethral and vaginal recovery after simulated vaginal delivery. Injection of stem cells induces faster recovery of urethral and vaginal function; cells overexpressing a factor increasing blood vessel formation, were even more effective.

2023-08-30 | GSE222561 | GEO

Trasncripional regulation by FOXO1 in Vascular Endothelial Cell Growth Factor (VEGF) treatment in human endothelial cells

Project description:FOXO1 was involved in various biologucal processes. In endothelial cells, it has reported that FOXO1 was phosphorylated by PI3K-Akt signaling, and it was nuclear exclusion by short-term VEGF stimulation. This event turns off the expression of apoptosis-related genes, it protects the cell from apoptosis. On the other hand, long-term VEGF stimulation, FOXO1 re-entry into the nucleus and induces the expression of different genes. Therefore, to identify genes regulated by FOXO1 in long-term VEGF stimulation, we performed RNA-seq analysis of FOXO1-knockdowned human unbilical vein endothelial cells (HUVECs) by siRNA and 18h VEGF treatment.

2024-03-01 | GSE220504 | GEO

Analysis of miRNA expression in lung (CC10) VEGF transgenic mice and their wild type litters

Project description:Vascular Endothelial Growth Factor (VEGF) is a critical regulator of pulmonary Th2 inflammation but the underlying mechanism and the roles of miRNAs in this process have not been defined. We analyzed the effect of VEGF on lung microRNAs by microarray analysis and validated the findings by Taqman qRT-PCR. We compared the levels of microRNAs in the lungs of transgenic mice with their wild type litters after overexpression of VEGF from a lung epithelium-restricted transgene. VEGF was overexpressed in the lung epithelium of CC10-rtTA-VEGF transgenic mice by adding Doxycycline to their drinking water for 7-10 days. RNA from the lungs of VEGF transgenic mice and their wild type litters were extracted and analyzed by microarray. The expression levels of microRNAs that were significanly altered were validated in another group of mice.

2013-09-06 | GSE50644 | GEO

VEGF-D deficiency causes hyperlipidemia and delayed clearance of chylomicron remnants

Project description:Objective: Dyslipidemia is one of the key factors behind coronary heart disease. Blood and lymphatic vessels play pivotal roles in both lipoprotein metabolism and development of atherosclerotic plaques. Recent studies have linked members of Vascular Endothelial Growth Factor (VEGF) family to lipid metabolism but the function of VEGF-D has remained unexplored. Here we investigated how the deletion of VEGF-D affects lipid and lipoprotein metabolism in atherogenic LDLR-/-ApoB100/100 mice. Approach and Results: Deletion of VEGF-D (Vegfd-/-LDLR-/-ApoB100/100) led to markedly elevated plasma cholesterol and triglyceride levels without an increase in atherogenesis. Size distribution and hepatic lipid uptake studies confirmed a delayed clearance of large chylomicron remnant particles that cannot easily penetrate through the vascular endothelium. Mechanistically, the inhibition of VEGF-D signaling significantly decreased the hepatic expression of syndecan 1 (SDC1), which is one of the main receptors for chylomicron remnant uptake when LDLR is absent. Immunohistochemical staining confirmed reduced expression of SDC1 in the sinusoidal surface of hepatocytes in VEGF-D deficient mice. Furthermore, hepatic RNA sequencing revealed that VEGF-D is also an important regulator of genes related to lipid metabolism and inflammation. The lack of VEGF-D signaling via VEGF receptor 3 led to lowered expression of genes regulating triglyceride and cholesterol production as well as downregulation of peroxisomal β-oxidation pathway. Conclusions: These results demonstrate that VEGF-D, a powerful lymphangiogenic and angiogenic growth factor, is also a major regulator of chylomicron metabolism in mice.

2018-08-16 | GSE108959 | GEO

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