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

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: GSE38455 | GEO | 2013/11/30

SECONDARY ACCESSION(S): PRJNA167974

REPOSITORIES: GEO

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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

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 VEGF-B transgenic rat hearts

2013-11-30 | GSE38454 | GEO

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

RNA sequencing of HUVECs stimulated with VEGF, OSM+VEGF, or CNTF+CNTFR+VEGF

Project description:RNA sequencing of HUVECs stimulated with VEGF, OSM+VEGF, or CNTF+CNTFR+VEGF

| PRJNA807293 | ENA

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

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

Adeno-associated viral vector delivers cardiac-specific and hypoxia-inducible VEGF expression in ischemic mouse hearts.

Project description:It has been shown that the adeno-associated virus (AAV) vector can deliver the VEGF gene efficiently into the ischemic mouse myocardium. However, the AAV genomes can be found in extracardiac organs after intramyocardial injection. To limit unwanted VEGF expression in organs other than the heart, we tested the use of the cardiac myosin light chain 2v (MLC-2v) promoter and the hypoxia-response element to mediate cardiac-specific and hypoxia-inducible VEGF expression. An AAV vector, MLCVEGF, with 250 bp of the MLC-2v promoter and nine copies of the hypoxia-response element driving VEGF expression, was constructed. Gene expression was studied in vitro by infection of rat cardiomyocytes, rat skeletal myocytes, and mouse fibroblasts with the vector and in vivo by direct injection of the vector into normal and ischemic mouse hearts. With MLCVEGF infection, VEGF expression was higher in cardiomyocytes than the other two cell lines and was hypoxiainducible. VEGF expression was also higher in ischemic hearts than in normal hearts. No VEGF expression was detectable in organs with detectable MLCVEGF vectors other than the heart. MLCVEGF-injected ischemic hearts had more capillaries and small vessels around the injection site, smaller infarct size, and better cardiac function than the negative controls. Hence, MLCVEGF can mediate cardiac-specific and hypoxia-inducible VEGF expression, neoangiogenesis, infarct-size reduction, and cardiac functional improvement.

| S-EPMC527136 | biostudies-literature

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