Single-cell RNA sequencing of mouse forebrain cells 5 weeks after injections of a control AAV9 or a VEGF-C/D trap AAV9
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PROVIDER: PRJNA962187 | ENA |
REPOSITORIES: ENA
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Project description:In this work we have induced meningeal lymphatic ablation by decreasing the circulating levels of VEGF-C and -D (VEGF-C/D trap), via injection of an AAV9 expressing domains 1 to 3 of murine VEGFR3 coupled to an Ig domain (VEGF-C/D trap). Control mice were injected with an AAV9 expressing domains 4 to 7 of murine VEGFR3 coupled to an Ig domain (controls). 5 weeks upon the initial injections, animals were perfused, and the forebrain tissue was collected and processed for single-cell RNA sequencing (10x Genomics).
2024-07-31 | GSE230709 | GEO
Project description:This phase II trial is studying how well VEGF Trap works in treating patients with previously treated metastatic colorectal cancer. VEGF Trap may stop the growth of colorectal cancer by blocking blood flow to the tumor.
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Project description:Regulation of neural stem cell (NSC) fate decisions is critical during the transition from a multicellular mammalian forebrain neuroepithelium to the multilayered neocortex. Forebrain development requires coordinated vascular investment alongside NSC differentiation. Vascular endothelial growth factor A (Vegf) has proven to be a pleiotrophic gene whose multiple protein isoforms regulate a broad range of effects in neurovascular systems. To test the hypothesis that the Vegf isoforms (120, 164, and 188) are required for normal forebrain development, we analyzed the forebrain transcriptome of mice expressing specific Vegf isoforms, Vegf120, VegfF188, or a combination of Vegf120/188. Transcriptome analysis identified differentially expressed genes in embryonic day (E) 9.5 forebrain, a time point preceding dramatic neuroepithelial expansion and vascular investment in the telencephalon. Meta-analysis identified gene pathways linked to chromosome-level modifications, cell fate regulation, and neurogenesis that were altered in Vegf isoform mice.
2013-11-21 | GSE52542 | GEO
Project description:Regulation of neural stem cell (NSC) fate decisions is critical during the transition from a multicellular mammalian forebrain neuroepithelium to the multilayered neocortex. Forebrain development requires coordinated vascular investment alongside NSC differentiation. Vascular endothelial growth factor A (Vegf) has proven to be a pleiotrophic gene whose multiple protein isoforms regulate a broad range of effects in neurovascular systems. To test the hypothesis that the Vegf isoforms (120, 164, and 188) are required for normal forebrain development, we analyzed the forebrain transcriptome of mice expressing specific Vegf isoforms, Vegf120, VegfF188, or a combination of Vegf120/188. Transcriptome analysis identified differentially expressed genes in embryonic day (E) 9.5 forebrain, a time point preceding dramatic neuroepithelial expansion and vascular investment in the telencephalon. Meta-analysis identified gene pathways linked to chromosome-level modifications, cell fate regulation, and neurogenesis that were altered in Vegf isoform mice. Twelve E9.5 wildtype forebrain samples were compared to four E9.5 Vegf120 mouse forebrains, four E9.5 Vegf188 mouse forebrains, three E9.5 Vegf120/188 mouse forebrains, and four E11.5 wild type forebrains using the Mouse 430. 2.0 Affymetrix GeneChip. This study comprises of new samples and reanalysis of Samples from GSE30767 and GSE8091.
2013-11-21 | E-GEOD-52542 | biostudies-arrayexpress
Project description:This work was designed to determine the role of the vascular endothelial growth factor A (VEGF) isoforms during early neuroepithelial development in the mammalian central nervous system (CNS), specifically in the forebrain. An emerging model of interdependence between neural and vascular systems includes VEGF, with its dual roles as a potent angiogenesis factor and neural regulator. Although a number of studies have implicated VEGF in CNS development, little is known about the role that the different VEGF isoforms play in early neurogenesis. We used a mouse model of disrupted VEGF isoform expression that eliminates the predominant brain isoform, VEGF164, and expresses only the diffusible form, VEGF120. We tested the hypothesis that VEGF164 plays a key role in controlling neural precursor populations in developing cortex. We used microarray analysis to compare gene expression differences between wild type and VEGF120 mice at E9.5, the primitive stem cell stage of the neuroepithelium. We quantified changes in PHH3-positive nuclei, neural stem cell markers (Pax6 and nestin) and the Tbr2-positive intermediate progenitors at E11.5 when the neural precursor population is expanding rapidly. Absence of VEGF164 (and VEGF188) leads to reduced proliferation without an apparent effect on the number of Tbr2-positive cells. There is a corresponding reduction in the number of mitotic spindles that are oriented parallel to the ventricular surface relative to those with a vertical or oblique angle. These results support a role for the VEGF isoforms in supporting the neural precursor population of the early neuroepithelium. Four samples each of E9.5 wildtype or VEGF120 mouse forebrain were analyzed with the Mouse 430 2.0 Affymetrix GeneChip
2011-12-01 | E-GEOD-30767 | biostudies-arrayexpress
Project description:This work was designed to determine the role of the vascular endothelial growth factor A (VEGF) isoforms during early neuroepithelial development in the mammalian central nervous system (CNS), specifically in the forebrain. An emerging model of interdependence between neural and vascular systems includes VEGF, with its dual roles as a potent angiogenesis factor and neural regulator. Although a number of studies have implicated VEGF in CNS development, little is known about the role that the different VEGF isoforms play in early neurogenesis. We used a mouse model of disrupted VEGF isoform expression that eliminates the predominant brain isoform, VEGF164, and expresses only the diffusible form, VEGF120. We tested the hypothesis that VEGF164 plays a key role in controlling neural precursor populations in developing cortex. We used microarray analysis to compare gene expression differences between wild type and VEGF120 mice at E9.5, the primitive stem cell stage of the neuroepithelium. We quantified changes in PHH3-positive nuclei, neural stem cell markers (Pax6 and nestin) and the Tbr2-positive intermediate progenitors at E11.5 when the neural precursor population is expanding rapidly. Absence of VEGF164 (and VEGF188) leads to reduced proliferation without an apparent effect on the number of Tbr2-positive cells. There is a corresponding reduction in the number of mitotic spindles that are oriented parallel to the ventricular surface relative to those with a vertical or oblique angle. These results support a role for the VEGF isoforms in supporting the neural precursor population of the early neuroepithelium.
2011-12-01 | GSE30767 | GEO
Project description:Transcriptional profiling of mouse liver was compared between VEGF inhibitor aflibercept and control treatment after 9 weeks. 8-10 week-old SCID mice received VEGF Trap protein (aflibercept) subcutaneously twice per week at 25mg per kg body weight for 9 weeks. For control groups, mice were treated with humanized Fc (Regeneron). 5 biological replicates were performed for the control group and 4 biological replicates were performed for the treatment group
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Project description:RNA sequencing of HUVECs stimulated with VEGF, OSM+VEGF, or CNTF+CNTFR+VEGF
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Project description:To investigate a potential therapeutic effect of ABTAA on NV-AMD, we employed a mouse model of laser-induced CNV, that mimics human NV-AMD. A laser photocoagulation on mouse retinas was performed to rupture RPE and Bruch’s membrane, and then the effects of ABTAA were compared with those of VEGF-Trap.
2018-10-01 | GSE88730 | GEO