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

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

PROVIDER: PRJNA433943 | ENA |

REPOSITORIES: ENA

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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

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

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

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Endothelial Rap1B mediates VEGF immunosuppression

Project description:Overcoming vascular immunosuppression: lack of endothelial cell (EC) responsiveness to inflammatory stimuli in the proangiogenic environment of tumors, is essential for successful cancer immunotherapy. The mechanisms through which Vascular Endothelial Growth Factor (VEGF) modulates tumor EC response to exclude T cells are not well understood. The goal was to determine the role of EC Rap1B, a small GTPase that positively regulates VEGF-angiogenesis during development, in tumor growth in vivo. Using mouse models of Rap1B deficiency, Rap1B+/- and endothelial-specific Rap1B KO (Rap1BiΔEC) we demonstrate Rap1B restricts tumor growth and angiogenesis. More importantly, EC-specific Rap1B deletion leads to an altered tumor microenvironment with increased recruitment of leukocytes and increased activity of tumor CD8+ T cells. We find that tumor growth, albeit not angiogenesis, is restored in Rap1BiΔEC mice by depleting CD8+ T cells. Mechanistically, global transcriptome analysis indicated upregulation of the TNF-α signaling and cytokine-induced NFκB transcriptional activity in Rap1B-deficient ECs. In particular, endothelial Rap1B deletion led to upregulation of Cell Adhesion Molecules (CAMs) expression in response to proinflammatory cytokines, and increased interaction with leukocytes in vitro. Importantly, deletion of Rap1 abrogated VEGF-mediated inhibition of CAM expression, demonstrating that Rap1B is essential for mediating VEGF-suppressive signaling. Thus, our studies identify a novel endothelial-endogenous mechanism underlying VEGF-dependent desensitization of EC to pro-inflammatory stimuli. Significantly, they identify EC Rap1 as a potential novel vascular target in cancer immunotherapy.

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Deletion of Trdn-as transcription in the adult heart.

Project description:Deletion of Trdn-as transcription in the adult heart.

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Deletion of Trdn-as transcription in the adult heart.

Project description:Deletion of Trdn-as transcription in the mouse heart reveals a function of trdn-as in the control of TRDN processing as well as secondary changes induced be the alteration of the cardiac calcium release complex.

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Project description:Meningeal lymphatic vessels (MLVs) promote tissue clearance and immune surveillance in the central nervous system (CNS). Vascular endothelial growth factor-C (VEGF-C) regulates MLV development and maintenance and has therapeutic potential for treating neurological disorders. Herein, we investigated the effects of VEGF-C overexpression on brain fluid drainage and ischemic stroke outcomes in mice. Intra-cerebrospinal administration of an adeno-associated virus expressing mouse full-length VEGF-C (AAV-mVEGF-C) increased CSF drainage to the deep cervical lymph nodes (dCLNs) by enhancing lymphatic growth, and upregulated neuroprotective signaling pathways identified by single nuclei RNA sequencing of brain cells. In a mouse model of ischemic stroke, AAV-mVEGF-C pretreatment reduced stroke injury and ameliorated motor performances in the subacute stage, associated with mitigated microglia-mediated inflammation and increased BDNF signaling in brain cells. Neuroprotective effects of VEGF-C were lost upon ligation of the dCLN afferent lymphatics, and not mimicked by acute post-stroke VEGF-C injection. We conclude that VEGF-C prophylaxis promotes multiple vascular, immune, and neural responses that culminate in a protection against neurological damage in acute ischemic stroke.

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