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yin198716新虫 (正式写手)
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Under physiological conditions, short-term administration ofg-secretase inhibitors (GSIs), which potently block Notch signaling, or pharmacological inhibition of Dll4/Notch interactions with a neutralizing antibody (Dll4-Fc) dramatically increases sprouting, branching, and filopodia formation at the leading front of the retinal vascular plexus in development, resulting in a much denser and more interconnected plexus 。The hypersprouting phenotype correlates with an increase in endothelial cells positive for the tip cell markers PDGFB or UNC5B and the number of endothelial filopodia protrusions, indicating increased tip cell formation in theabsence of Notch signaling ). Similar effects have been reported in the postnatal mouse retina and embryonic hindbrain vascularization after genetic deletion of one Dll4 allele or endothelial-specific Notch1 loss of function . Both the pharmacological inhibition and genetic studies illustrate that the Dll4/ Notch pathway critically regulates the formation of an adequate ratio of tip and stalk cells by suppressing tip cell formation in adjacent cells. Notch gain-of-function studies further support this idea; activation of Notch signaling using a synthetic Jagged1 ligand peptide reduces filopodia formation and branching, suggesting a decrease in the number of endothelial cells that acquire tip cell behavio. |
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