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10.1242/dev.135392 http://scihub22266oqcxt.onion/10.1242/dev.135392 C4958337!4958337!27287800     free     free     free 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       Development 2016 ; 143 (14): 2593-602 Nephropedia Template TP {{tp|p=27287800|t=2016. Alk1 controls arterial endothelial cell migration in lumenized vessels |pdf=|usr=}}{{27287800}} gab.com Text Alk1 controls arterial endothelial cell migration in lumenized vessels JO: Development http://www.kidney.de/pget.php?&tw=1&pmid=27287800 #FOAvip Heterozygous loss of the arterial-specific TGF? type I receptor, activin receptor-like kinase 1 (ALK1; ACVRL1), causes hereditary hemorrhagic telangiectasia (HHT). HHT is characterized by development of fragile, direct connections between arteries and veins, or arteriovenous malformations (AVMs). However, how decreased ALK1 signaling leads to AVMs is unknown. To understand the cellular mis-steps that cause AVMs, we assessed endothelial cell behavior in alk1-deficient zebrafish embryos, which develop cranial AVMs. Our data demonstrate that alk1 loss has no effect on arterial endothelial cell proliferation but alters arterial endothelial cell migration within lumenized vessels. In wild-type embryos, alk1-positive cranial arterial endothelial cells generally migrate towards the heart, against the direction of blood flow, with some cells incorporating into endocardium. In alk1-deficient embryos, migration against flow is dampened and migration in the direction of flow is enhanced. Altered migration results in decreased endothelial cell number in arterial segments proximal to the heart and increased endothelial cell number in arterial segments distal to the heart. We speculate that the consequent increase in distal arterial caliber and hemodynamic load precipitates the flow-dependent development of downstream AVMs. Twit Text FOAVip Alk1 controls arterial endothelial cell migration in lumenized vessels ????Development http://www.kidney.de/pget.php?&tw=1&pmid=27287800 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27287800 #FOAvip English Wikipedia <ref>{{Cite pmid|27287800}}</ref> Alk1 controls arterial endothelial cell migration in lumenized vessels #MMPMID27287800 Rochon ER; Menon PG; Roman BL Development 2016[Jul]; 143 (14): 2593-602 PMID27287800show ga Heterozygous loss of the arterial-specific TGF? type I receptor, activin receptor-like kinase 1 (ALK1; ACVRL1), causes hereditary hemorrhagic telangiectasia (HHT). HHT is characterized by development of fragile, direct connections between arteries and veins, or arteriovenous malformations (AVMs). However, how decreased ALK1 signaling leads to AVMs is unknown. To understand the cellular mis-steps that cause AVMs, we assessed endothelial cell behavior in alk1-deficient zebrafish embryos, which develop cranial AVMs. Our data demonstrate that alk1 loss has no effect on arterial endothelial cell proliferation but alters arterial endothelial cell migration within lumenized vessels. In wild-type embryos, alk1-positive cranial arterial endothelial cells generally migrate towards the heart, against the direction of blood flow, with some cells incorporating into endocardium. In alk1-deficient embryos, migration against flow is dampened and migration in the direction of flow is enhanced. Altered migration results in decreased endothelial cell number in arterial segments proximal to the heart and increased endothelial cell number in arterial segments distal to the heart. We speculate that the consequent increase in distal arterial caliber and hemodynamic load precipitates the flow-dependent development of downstream AVMs. äAlk1 controls arterial endothelial cell migration in lumenized vessels(epmc).pdf DeepDyve Pubget Overpricing