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10.1161/ATVBAHA.113.301805 http://scihub22266oqcxt.onion/10.1161/ATVBAHA.113.301805 C4521230!4521230 !23744993     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=23744993 &cmd=llinks): Failed to open stream: HTTP request failed! 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Flt-1 (vascular endothelial growth factor receptor-1) is essential for the vascular endothelial growth factor-Notch feedback loop during angiogenesis |pdf=|usr=}}{{23744993 }} gab.com Text Flt-1 (vascular endothelial growth factor receptor-1) is essential for the vascular endothelial growth factor-Notch feedback loop during angiogenesis JO: Arterioscler Thromb Vasc Biol http://www.kidney.de/pget.php?&tw=1&pmid=23744993 #FOAvip OBJECTIVE: Vascular endothelial growth factor (VEGF) signaling induces Notch signaling during angiogenesis. Flt-1/VEGF receptor-1 negatively modulates VEGF signaling. Therefore, we tested the hypothesis that disrupted Flt-1 regulation of VEGF signaling causes Notch pathway defects that contribute to dysmorphogenesis of Flt-1 mutant vessels. APPROACH AND RESULTS: Wild-type and flt-1(-/-) mouse embryonic stem cell-derived vessels were exposed to pharmacological and protein-based Notch inhibitors with and without added VEGF. Vessel morphology, endothelial cell proliferation, and Notch target gene expression levels were assessed. Similar pathway manipulations were performed in developing vessels of zebrafish embryos. Notch inhibition reduced flt-1(-/-) embryonic stem cell-derived vessel branching dysmorphogenesis and endothelial hyperproliferation, and rescue of flt-1(-/-) vessels was accompanied by a reduction in elevated Notch targets. Surprisingly, wild-type vessel morphogenesis and proliferation were unaffected by Notch suppression, Notch targets in wild-type endothelium were unchanged, and Notch suppression perturbed zebrafish intersegmental vessels but not caudal vein plexuses. In contrast, exogenous VEGF caused wild-type embryonic stem cell-derived vessel and zebrafish intersegmental vessel dysmorphogenesis that was rescued by Notch blockade. CONCLUSIONS: Elevated Notch signaling downstream of perturbed VEGF signaling contributes to aberrant flt-1(-/-) blood vessel formation. Notch signaling may be dispensable for blood vessel formation when VEGF signaling is below a critical threshold. Twit Text FOAVip Flt-1 (vascular endothelial growth factor receptor-1) is essential for the vascular endothelial growth factor-Notch feedback loop during angiogenesis ????Arterioscler Thromb Vasc Biol http://www.kidney.de/pget.php?&tw=1&pmid=23744993 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23744993 #FOAvip English Wikipedia <ref>{{Cite pmid|23744993 }}</ref> Flt-1 (vascular endothelial growth factor receptor-1) is essential for the vascular endothelial growth factor-Notch feedback loop during angiogenesis #MMPMID23744993 Chappell JC ; Mouillesseaux KP ; Bautch VL Arterioscler Thromb Vasc Biol 2013[Aug]; 33 (8 ): 1952-9 PMID23744993 show ga OBJECTIVE: Vascular endothelial growth factor (VEGF) signaling induces Notch signaling during angiogenesis. Flt-1/VEGF receptor-1 negatively modulates VEGF signaling. Therefore, we tested the hypothesis that disrupted Flt-1 regulation of VEGF signaling causes Notch pathway defects that contribute to dysmorphogenesis of Flt-1 mutant vessels. APPROACH AND RESULTS: Wild-type and flt-1(-/-) mouse embryonic stem cell-derived vessels were exposed to pharmacological and protein-based Notch inhibitors with and without added VEGF. Vessel morphology, endothelial cell proliferation, and Notch target gene expression levels were assessed. Similar pathway manipulations were performed in developing vessels of zebrafish embryos. Notch inhibition reduced flt-1(-/-) embryonic stem cell-derived vessel branching dysmorphogenesis and endothelial hyperproliferation, and rescue of flt-1(-/-) vessels was accompanied by a reduction in elevated Notch targets. Surprisingly, wild-type vessel morphogenesis and proliferation were unaffected by Notch suppression, Notch targets in wild-type endothelium were unchanged, and Notch suppression perturbed zebrafish intersegmental vessels but not caudal vein plexuses. In contrast, exogenous VEGF caused wild-type embryonic stem cell-derived vessel and zebrafish intersegmental vessel dysmorphogenesis that was rescued by Notch blockade. CONCLUSIONS: Elevated Notch signaling downstream of perturbed VEGF signaling contributes to aberrant flt-1(-/-) blood vessel formation. Notch signaling may be dispensable for blood vessel formation when VEGF signaling is below a critical threshold. |Amyloid Precursor Protein Secretases/antagonists & inhibitors [MESH] |Animals [MESH] |Cell Proliferation [MESH] |Dipeptides/pharmacology [MESH] |Embryonic Stem Cells/metabolism [MESH] |Endothelium, Vascular/abnormalities/embryology/metabolism [MESH] |Feedback, Physiological/drug effects/physiology [MESH] |Gene Expression Regulation, Developmental/physiology [MESH] |Mice [MESH] |Mice, Knockout [MESH] |Neovascularization, Physiologic/*physiology [MESH] |Receptors, Notch/antagonists & inhibitors/*metabolism [MESH] |Signal Transduction/drug effects/*physiology [MESH] |Vascular Endothelial Growth Factor A/*metabolism [MESH] |Vascular Endothelial Growth Factor Receptor-1/genetics/*metabolism [MESH] |Veins/abnormalities/embryology/metabolism [MESH] |Zebrafish [MESH]Flt-1 (vascular endothelial growth factor receptor-1) is essential for(epmc).pdf DeepDyve Pubget Overpricing