A genetic Xenopus laevis tadpole model to study lymphangiogenesis.
Identifieur interne : 003C21 ( PubMed/Corpus ); précédent : 003C20; suivant : 003C22A genetic Xenopus laevis tadpole model to study lymphangiogenesis.
Auteurs : Annelii Ny ; Marta Koch ; Martin Schneider ; Elke Neven ; Ricky T. Tong ; Sunit Maity ; Christian Fischer ; Stephane Plaisance ; Diether Lambrechts ; Christophe Héligon ; Sven Terclavers ; Malgorzata Ciesiolka ; Roland K Lin ; Wing Yan Man ; Irena Senn ; Sabine Wyns ; Florea Lupu ; André Br Ndli ; Kris Vleminckx ; Désiré Collen ; Mieke Dewerchin ; Edward M. Conway ; Lieve Moons ; Rakesh K. Jain ; Peter CarmelietSource :
- Nature medicine [ 1078-8956 ] ; 2005.
English descriptors
- KwdEn :
- Animals, Homeodomain Proteins (physiology), Larva (genetics), Larva (growth & development), Lymphangiogenesis (genetics), Lymphangiogenesis (physiology), Lymphatic System (anatomy & histology), Lymphatic System (growth & development), Tumor Suppressor Proteins, Xenopus laevis (genetics), Xenopus laevis (growth & development).
- MESH :
- chemical , physiology : Homeodomain Proteins.
- anatomy & histology : Lymphatic System.
- genetics : Larva, Lymphangiogenesis, Xenopus laevis.
- growth & development : Larva, Lymphatic System, Xenopus laevis.
- physiology : Lymphangiogenesis.
- Animals, Tumor Suppressor Proteins.
Abstract
Lymph vessels control fluid homeostasis, immunity and metastasis. Unraveling the molecular basis of lymphangiogenesis has been hampered by the lack of a small animal model that can be genetically manipulated. Here, we show that Xenopus tadpoles develop lymph vessels from lymphangioblasts or, through transdifferentiation, from venous endothelial cells. Lymphangiography showed that these lymph vessels drain lymph, through the lymph heart, to the venous circulation. Morpholino-mediated knockdown of the lymphangiogenic factor Prox1 caused lymph vessel defects and lymphedema by impairing lymphatic commitment. Knockdown of vascular endothelial growth factor C (VEGF-C) also induced lymph vessel defects and lymphedema, but primarily by affecting migration of lymphatic endothelial cells. Knockdown of VEGF-C also resulted in aberrant blood vessel formation in tadpoles. This tadpole model offers opportunities for the discovery of new regulators of lymphangiogenesis.
DOI: 10.1038/nm1285
PubMed: 16116431
Links to Exploration step
pubmed:16116431Le document en format XML
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<front><div type="abstract" xml:lang="en">Lymph vessels control fluid homeostasis, immunity and metastasis. Unraveling the molecular basis of lymphangiogenesis has been hampered by the lack of a small animal model that can be genetically manipulated. Here, we show that Xenopus tadpoles develop lymph vessels from lymphangioblasts or, through transdifferentiation, from venous endothelial cells. Lymphangiography showed that these lymph vessels drain lymph, through the lymph heart, to the venous circulation. Morpholino-mediated knockdown of the lymphangiogenic factor Prox1 caused lymph vessel defects and lymphedema by impairing lymphatic commitment. Knockdown of vascular endothelial growth factor C (VEGF-C) also induced lymph vessel defects and lymphedema, but primarily by affecting migration of lymphatic endothelial cells. Knockdown of VEGF-C also resulted in aberrant blood vessel formation in tadpoles. This tadpole model offers opportunities for the discovery of new regulators of lymphangiogenesis.</div>
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<Abstract><AbstractText>Lymph vessels control fluid homeostasis, immunity and metastasis. Unraveling the molecular basis of lymphangiogenesis has been hampered by the lack of a small animal model that can be genetically manipulated. Here, we show that Xenopus tadpoles develop lymph vessels from lymphangioblasts or, through transdifferentiation, from venous endothelial cells. Lymphangiography showed that these lymph vessels drain lymph, through the lymph heart, to the venous circulation. Morpholino-mediated knockdown of the lymphangiogenic factor Prox1 caused lymph vessel defects and lymphedema by impairing lymphatic commitment. Knockdown of vascular endothelial growth factor C (VEGF-C) also induced lymph vessel defects and lymphedema, but primarily by affecting migration of lymphatic endothelial cells. Knockdown of VEGF-C also resulted in aberrant blood vessel formation in tadpoles. This tadpole model offers opportunities for the discovery of new regulators of lymphangiogenesis.</AbstractText>
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