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10.1242/dev.145672 http://scihub22266oqcxt.onion/10.1242/dev.145672 C5374355!5374355!28246215     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Development 2017 ; 144 (5): 889-96 Nephropedia Template TP {{tp|p=28246215|t=2017. Blood vessel anastomosis is spatially regulated by Flt1 during angiogenesis |pdf=|usr=}}{{28246215}} gab.com Text Blood vessel anastomosis is spatially regulated by Flt1 during angiogenesis JO: Development http://www.kidney.de/pget.php?&tw=1&pmid=28246215 #FOAvip Blood vessel formation is essential for vertebrate development and is primarily achieved by angiogenesis ? endothelial cell sprouting from pre-existing vessels. Vessel networks expand when sprouts form new connections, a process whose regulation is poorly understood. Here, we show that vessel anastomosis is spatially regulated by Flt1 (VEGFR1), a VEGFA receptor that acts as a decoy receptor. In vivo, expanding vessel networks favor interactions with Flt1 mutant mouse endothelial cells. Live imaging in human endothelial cells in vitro revealed that stable connections are preceded by transient contacts from extending sprouts, suggesting sampling of potential target sites, and lowered Flt1 levels reduced transient contacts and increased VEGFA signaling. Endothelial cells at target sites with reduced Flt1 and/or elevated protrusive activity were more likely to form stable connections with incoming sprouts. Target cells with reduced membrane-localized Flt1 (mFlt1), but not soluble Flt1, recapitulated the bias towards stable connections, suggesting that relative mFlt1 expression spatially influences the selection of stable connections. Thus, sprout anastomosis parameters are regulated by VEGFA signaling, and stable connections are spatially regulated by endothelial cell-intrinsic modulation of mFlt1, suggesting new ways to manipulate vessel network formation. Twit Text FOAVip Blood vessel anastomosis is spatially regulated by Flt1 during angiogenesis ????Development http://www.kidney.de/pget.php?&tw=1&pmid=28246215 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28246215 #FOAvip English Wikipedia <ref>{{Cite pmid|28246215}}</ref> Blood vessel anastomosis is spatially regulated by Flt1 during angiogenesis #MMPMID28246215 Nesmith JE; Chappell JC; Cluceru JG; Bautch VL Development 2017[Mar]; 144 (5): 889-96 PMID28246215show ga Blood vessel formation is essential for vertebrate development and is primarily achieved by angiogenesis ? endothelial cell sprouting from pre-existing vessels. Vessel networks expand when sprouts form new connections, a process whose regulation is poorly understood. Here, we show that vessel anastomosis is spatially regulated by Flt1 (VEGFR1), a VEGFA receptor that acts as a decoy receptor. In vivo, expanding vessel networks favor interactions with Flt1 mutant mouse endothelial cells. Live imaging in human endothelial cells in vitro revealed that stable connections are preceded by transient contacts from extending sprouts, suggesting sampling of potential target sites, and lowered Flt1 levels reduced transient contacts and increased VEGFA signaling. Endothelial cells at target sites with reduced Flt1 and/or elevated protrusive activity were more likely to form stable connections with incoming sprouts. Target cells with reduced membrane-localized Flt1 (mFlt1), but not soluble Flt1, recapitulated the bias towards stable connections, suggesting that relative mFlt1 expression spatially influences the selection of stable connections. Thus, sprout anastomosis parameters are regulated by VEGFA signaling, and stable connections are spatially regulated by endothelial cell-intrinsic modulation of mFlt1, suggesting new ways to manipulate vessel network formation. äBlood vessel anastomosis is spatially regulated by Flt1 during angioge(epmc).pdf DeepDyve Pubget Overpricing