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- W3169236078 abstract "Paracrine-derived vascular endothelial growth factor (VEGF) is established as an indispensable contributor to the angiogenic cascade. Autocrine VEGF, in contrast, is solely attributed to endothelial cell survival signaling, and its potential regulation of other endothelial cell functions has not been studied. We hypothesized that the deletion of VEGF would disrupt endothelial cell migration and shear stress adaptation. Endothelial cells were isolated from transgenic mice having VEGF exon 3 flanked by loxP sites (VEGFL/L). Cells were transduced with adeno-Cre recombinase to induce VEGF deletion, or adeno-β-galactosidase as a control. When subjected to a scrape migration assay, cells with Cre induced VEGF deletion (VEGFΔ) exhibited impaired cell motility compared VEGFL/L cells (12% compared to 64% wound closure after 48 hours; p<0.05). Shear stress stimulation (15 dynes; 2hr) caused significant increases in phospho-Akt in VEGFL/L cells, which was repressed in VEGFΔ cells (2.4 vs. 1.5 fold above static, respectively). Shear-induced increases in phospho-p38MAPK were unaltered in VEGFΔ cells (3.9 vs 3.3 fold above static, respectively). Shear-induced endothelial cell alignment (15 dynes; 24hr) also was repressed in VEGFΔ cells. Taken together these results provide novel evidence that autocrine VEGF contributes to multiple aspects of endothelial cell function." @default.
- W3169236078 created "2021-06-22" @default.
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- W3169236078 date "2013-04-01" @default.
- W3169236078 modified "2023-09-28" @default.
- W3169236078 title "A potential role for autocrine VEGF signaling in endothelial cell function" @default.
- W3169236078 doi "https://doi.org/10.1096/fasebj.27.1_supplement.685.14" @default.
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