a phosphoinositide 3-kinasephospholipase cgamma1 pathway regulates fibroblast growth factor-induced capillary tube formation一磷酸肌醇3-kinasephospholipase cgamma1通路调节纤维母细胞生长因素毛细管的形成.pdfVIP

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a phosphoinositide 3-kinasephospholipase cgamma1 pathway regulates fibroblast growth factor-induced capillary tube formation一磷酸肌醇3-kinasephospholipase cgamma1通路调节纤维母细胞生长因素毛细管的形成.pdf

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a phosphoinositide 3-kinasephospholipase cgamma1 pathway regulates fibroblast growth factor-induced capillary tube formation一磷酸肌醇3-kinasephospholipase cgamma1通路调节纤维母细胞生长因素毛细管的形成

A Phosphoinositide 3-Kinase/Phospholipase Cgamma1 Pathway Regulates Fibroblast Growth Factor-Induced Capillary Tube Formation 1 1 2 1 1 Tania Maffucci , Claudio Raimondi , Shadi Abu-Hayyeh , Veronica Dominguez , Gianluca Sala , Ian 2 1 Zachary , Marco Falasca * 1 Queen Mary University of London, Barts and The London School of Medicine and Dentistry, Blizard Institute of Cell and Molecular Science, Centre for Diabetes, Inositide Signalling Group, London, United Kingdom, 2 Department of Medicine, British Heart Foundation Laboratories, Centre for Cardiovascular Biology and Medicine, University College London, London, United Kingdom Abstract Background: The fibroblast growth factors (FGFs) are key regulators of embryonic development, tissue homeostasis and tumour angiogenesis. Binding of FGFs to their receptor(s) results in activation of several intracellular signalling cascades including phosphoinositide 3-kinase (PI3K) and phospholipase C (PLC)c1. Here we investigated the basic FGF (FGF-2)- mediated activation of these enzymes in human umbilical vein endothelial cells (HUVECs) and defined their role in FGF-2- dependent cellular functions. Methodology/Principal Findings: We show that FGF-2 activates PLCc1 in HUVECs measured by analysis of total inositol phosphates production upon metabolic labelling of cells and intracellular calcium increase. We further demonstrate that FGF-2 activates PI3K, assessed by analysing accumulation of its lipid product phosphatidylinositol-3,4,5-P3 using TLC and confocal microscopy analysis. PI3K activity is required for FGF-2-induced PLCc1 activation and the PI3K/PLCc1 pathway is involved in FGF-2-dependent cell migration, determined