Rapamycin improves TIE2-mutated venous malformation in murine model and human subjects

Venous malformations (VMs) are composed of ectatic veins with scarce smooth muscle cell coverage. Activating mutations in the endothelial cell tyrosine kinase receptor TIE2 are a common cause of these lesions. VMs cause deformity, pain, and local intravascular coagulopathy, and they expand with time...

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Bibliographic Details
Published in:	The Journal of clinical investigation Vol. 125; no. 9; pp. 3491 - 3504
Main Authors:	Boscolo, Elisa, Limaye, Nisha, Huang, Lan, Kang, Kyu-Tae, Soblet, Julie, Uebelhoer, Melanie, Mendola, Antonella, Natynki, Marjut, Seront, Emmanuel, Dupont, Sophie, Hammer, Jennifer, Legrand, Catherine, Brugnara, Carlo, Eklund, Lauri, Vikkula, Miikka, Bischoff, Joyce, Boon, Laurence M.
Format:	Journal Article
Language:	English
Published:	United States American Society for Clinical Investigation 01.09.2015
Subjects:	Adolescent Adult Analysis Animal models in research Animals Biomedical research Disease Models, Animal Drug therapy Female Genetic aspects Health aspects Human Umbilical Vein Endothelial Cells - metabolism Human Umbilical Vein Endothelial Cells - pathology Humans Immunosuppressive Agents - administration & dosage Male Mice Mice, Nude Middle Aged Mutation Mutation, Missense Patients Phosphorylation Pilot Projects Proto-Oncogene Proteins c-akt - genetics Proto-Oncogene Proteins c-akt - metabolism Rapamycin Receptor, TIE-2 - genetics Receptor, TIE-2 - metabolism Risk factors Signal Transduction - drug effects Signal Transduction - genetics Sirolimus - administration & dosage Vascular Malformations - drug therapy Vascular Malformations - genetics Vascular Malformations - metabolism Vascular Malformations - pathology Veins Venous insufficiency Belgium
ISSN:	0021-9738, 1558-8238
Online Access:	Get full text
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