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• W4362473235 abstract "Dynamic positioning of endothelial tip and stalk cells, via the interplay between VEGFR2 and NOTCH signaling, is essential for angiogenesis. VEGFR2 activates PI3K, which phosphorylates PI(4,5)P2 to PI(3,4,5)P3, activating AKT; however, PI3K/AKT does not direct tip cell specification. We report that PI(4,5)P2 hydrolysis by the phosphoinositide-5-phosphatase, INPP5K, contributes to angiogenesis. INPP5K ablation disrupted tip cell specification and impaired embryonic angiogenesis associated with enhanced DLL4/NOTCH signaling. INPP5K degraded a pool of PI(4,5)P2 generated by PIP5K1C phosphorylation of PI(4)P in endothelial cells. INPP5K ablation increased PI(4,5)P2, thereby releasing β-catenin from the plasma membrane, and concurrently increased PI(3,4,5)P3-dependent AKT activation, conditions that licensed DLL4/NOTCH transcription. Suppression of PI(4,5)P2 in INPP5K-siRNA cells by PIP5K1C-siRNA, restored β-catenin membrane localization and normalized AKT signaling. Pharmacological NOTCH or AKT inhibition in vivo or genetic β-catenin attenuation rescued angiogenesis defects in INPP5K-null mice. Therefore, PI(4,5)P2 is critical for β-catenin/DLL4/NOTCH signaling, which governs tip cell specification during angiogenesis." @default.
• W4362473235 created "2023-04-05" @default.
• W4362473235 creator A5000827967 @default.
• W4362473235 creator A5021654311 @default.
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• W4362473235 creator A5048353848 @default.
• W4362473235 creator A5050050999 @default.
• W4362473235 creator A5050363590 @default.
• W4362473235 creator A5061644579 @default.
• W4362473235 creator A5061874736 @default.
• W4362473235 date "2023-03-31" @default.
• W4362473235 modified "2023-10-06" @default.
• W4362473235 title "PI(4,5)P ₂ -dependent regulation of endothelial tip cell specification contributes to angiogenesis" @default.
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