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Vammin induces a highly efficient angiogenic response through VEGFR-2/NRP-1 and bypasses the regulatory function of VEGFR-1

ABSTRACT: Rationale: VEGF family members mediate their effects through cell surface receptors VEGFR-1, VEGFR-2 and NRP. Specific ligands were used to stimulate specific combinations of the receptors to evaluate ligand and receptor properties. Objective: The properties of a novel VEGF family member Vammin were studied in level of receptor binding, gene expression in HUVECs by RNAseq and in vivo using adenoviral gene trasfers. Methods: HUVECs were trasduced using adenoviral vectors encoding VEGF-A109, VEGF-A165 and Vammin and with an empty vector as a control. Gene expression was measured using RNA sequencing. Adenoviral intramuscular gene transfers were performed into rabbit hindlimbs. Confocal and multiphoton microscopy were used for blood vessel imaging. Results and conclusions: Vammin is a highly effective VEGFR2 ligand that induces differential gene expression of genes related to proliferation, survival, angiogenesis and blood vessel development in HUVECs. The effect is stronger than ones induced by VEGF-A165 and VEGF-A109. Vammin induces highly efficient angiogenic responses when delivered into rabbit skeletal muscles using adenoviral gene transfers.

ORGANISM(S): Homo sapiens

PROVIDER: GSE68535 | GEO | 2017/08/11

SECONDARY ACCESSION(S): PRJNA283028

REPOSITORIES: GEO

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Slit2 modifies VEGF-induced angiogenic responses in rabbit skeletal muscle by inducing capillary sprouting and decreasing vascular permeability via reduced eNOS activity

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Slit2 modifies VEGF-induced angiogenic responses in rabbit skeletal muscle by inducing capillary sprouting and decreasing vascular permeability via reduced eNOS activity

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VEGFR-1 expressed by malignant melanoma initiating cells is required for tumor growth

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VEGFR-1 expressed by malignant melanoma initiating cells is required for tumor growth

2011-01-13 | E-GEOD-26569 | biostudies-arrayexpress

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Transcription profiling of human umbilical vein endothelial cells (HUVEC) treated with VEGF-A

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