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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! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Arterioscler+Thromb+Vasc+Biol 2013 ; 33 (8): 1952-9 Nephropedia Template TP {{tp|p=23744993|t=2013. Flt-1 (VEGFR-1) is Essential for the VEGF-Notch Feedback Loop during Angiogenesis |pdf=|usr=}}{{23744993}} gab.com Text Flt-1 (VEGFR-1) is Essential for the VEGF-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 (VEGFR-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 (WT) and flt-1?/? mouse embryonic stem (ES) 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?/? ES cell-derived vessel branching dysmorphogenesis and endothelial hyper-proliferation, and rescue of flt-1?/? vessels was accompanied by a reduction of elevated Notch targets. Surprisingly, WT vessel morphogenesis and proliferation were unaffected by Notch suppression, Notch targets in WT endothelium were unchanged, and Notch suppression perturbed zebrafish intersegmental vessels (ISVs) but not caudal vein plexuses (CVPs). In contrast, exogenous VEGF caused WT ES cell-derived vessel and zebrafish ISV 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 (VEGFR-1) is Essential for the VEGF-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 (VEGFR-1) is Essential for the VEGF-Notch Feedback Loop during Angiogenesis #MMPMID23744993 Chappell JC; Mouillesseaux KP; Bautch VL Arterioscler Thromb Vasc Biol 2013[Aug]; 33 (8): 1952-9 PMID23744993show ga Objective: Vascular endothelial growth factor (VEGF) signaling induces Notch signaling during angiogenesis. Flt-1/VEGF receptor-1 (VEGFR-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 (WT) and flt-1?/? mouse embryonic stem (ES) 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?/? ES cell-derived vessel branching dysmorphogenesis and endothelial hyper-proliferation, and rescue of flt-1?/? vessels was accompanied by a reduction of elevated Notch targets. Surprisingly, WT vessel morphogenesis and proliferation were unaffected by Notch suppression, Notch targets in WT endothelium were unchanged, and Notch suppression perturbed zebrafish intersegmental vessels (ISVs) but not caudal vein plexuses (CVPs). In contrast, exogenous VEGF caused WT ES cell-derived vessel and zebrafish ISV 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. äFlt-1 (VEGFR-1) is Essential for the VEGF-Notch Feedback Loop during A(epmc).pdf DeepDyve Pubget Overpricing