Angiopoietin-4 increases permeability of blood vessels and promotes lymphatic dilation
Identifieur interne : 002150 ( Main/Merge ); précédent : 002149; suivant : 002151Angiopoietin-4 increases permeability of blood vessels and promotes lymphatic dilation
Auteurs : Cristina T. Kesler ; Ethel R. Pereira ; Cheryl H. Cui ; Gregory M. Nelson ; David J. Masuck ; James W. Baish ; Timothy P. PaderaSource :
- The FASEB Journal [ 0892-6638 ] ; 2015.
Descripteurs français
- KwdFr :
- Angiopoïétines (génétique), Angiopoïétines (métabolisme), Animaux, Cellules endothéliales (anatomopathologie), Cellules endothéliales (métabolisme), Facteur de croissance endothéliale vasculaire de type C (génétique), Facteur de croissance endothéliale vasculaire de type C (métabolisme), Fibrosarcome (anatomopathologie), Fibrosarcome (génétique), Fibrosarcome (métabolisme), Humains, Mitogen-Activated Protein Kinase 1 (génétique), Mitogen-Activated Protein Kinase 1 (métabolisme), Mitogen-Activated Protein Kinase 3 (génétique), Mitogen-Activated Protein Kinase 3 (métabolisme), Néovascularisation pathologique (anatomopathologie), Néovascularisation pathologique (génétique), Néovascularisation pathologique (métabolisme), Perméabilité capillaire, Souris, Souris nude, Tumeurs expérimentales (anatomopathologie), Tumeurs expérimentales (génétique), Tumeurs expérimentales (métabolisme), Vaisseaux lymphatiques (anatomopathologie), Vaisseaux lymphatiques (métabolisme).
- MESH :
- anatomopathologie : Cellules endothéliales, Fibrosarcome, Néovascularisation pathologique, Tumeurs expérimentales, Vaisseaux lymphatiques.
- génétique : Angiopoïétines, Facteur de croissance endothéliale vasculaire de type C, Fibrosarcome, Mitogen-Activated Protein Kinase 1, Mitogen-Activated Protein Kinase 3, Néovascularisation pathologique, Tumeurs expérimentales.
- métabolisme : Angiopoïétines, Cellules endothéliales, Facteur de croissance endothéliale vasculaire de type C, Fibrosarcome, Mitogen-Activated Protein Kinase 1, Mitogen-Activated Protein Kinase 3, Néovascularisation pathologique, Tumeurs expérimentales, Vaisseaux lymphatiques.
- Animaux, Humains, Perméabilité capillaire, Souris, Souris nude.
English descriptors
- KwdEn :
- Angiopoietins (genetics), Angiopoietins (metabolism), Animals, Capillary Permeability, Endothelial Cells (metabolism), Endothelial Cells (pathology), Fibrosarcoma (genetics), Fibrosarcoma (metabolism), Fibrosarcoma (pathology), Humans, Lymphatic Vessels (metabolism), Lymphatic Vessels (pathology), Mice, Mice, Nude, Mitogen-Activated Protein Kinase 1 (genetics), Mitogen-Activated Protein Kinase 1 (metabolism), Mitogen-Activated Protein Kinase 3 (genetics), Mitogen-Activated Protein Kinase 3 (metabolism), Neoplasms, Experimental (genetics), Neoplasms, Experimental (metabolism), Neoplasms, Experimental (pathology), Neovascularization, Pathologic (genetics), Neovascularization, Pathologic (metabolism), Neovascularization, Pathologic (pathology), Vascular Endothelial Growth Factor C (genetics), Vascular Endothelial Growth Factor C (metabolism).
- MESH :
- chemical , genetics : Angiopoietins, Mitogen-Activated Protein Kinase 1, Mitogen-Activated Protein Kinase 3, Vascular Endothelial Growth Factor C.
- chemical , metabolism : Angiopoietins, Mitogen-Activated Protein Kinase 1, Mitogen-Activated Protein Kinase 3, Vascular Endothelial Growth Factor C.
- genetics : Fibrosarcoma, Neoplasms, Experimental, Neovascularization, Pathologic.
- metabolism : Endothelial Cells, Fibrosarcoma, Lymphatic Vessels, Neoplasms, Experimental, Neovascularization, Pathologic.
- pathology : Endothelial Cells, Fibrosarcoma, Lymphatic Vessels, Neoplasms, Experimental, Neovascularization, Pathologic.
- Animals, Capillary Permeability, Humans, Mice, Mice, Nude.
Abstract
The angiopoietin (Ang) ligands are potential therapeutic targets for lymphatic related diseases, which include lymphedema and cancer. Ang-1 and Ang-2 functions are established, but those of Ang-4 are poorly understood. We used intravital fluorescence microscopy to characterize Ang-4 actions on T241 murine fibrosarcoma-associated vessels in mice. The diameters of lymphatic vessels draining Ang-4- or VEGF-C (positive control)-expressing tumors increased to 123 and 135 μm, respectively, and parental, mock-transduced (negative controls) and tumors expressing Ang-1 or Ang-2 remained at baseline (∼60 μm). Ang-4 decreased human dermal lymphatic endothelial cell (LEC) monolayer permeability by 27% while increasing human dermal blood endothelial cell (BEC) monolayer permeability by 200%.
Url:
DOI: 10.1096/fj.14-268920
PubMed: 25977256
PubMed Central: 4550378
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PMC:4550378Le document en format XML
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Angiopoietins (genetics)</term>
<term>Angiopoietins (metabolism)</term>
<term>Animals</term>
<term>Capillary Permeability</term>
<term>Endothelial Cells (metabolism)</term>
<term>Endothelial Cells (pathology)</term>
<term>Fibrosarcoma (genetics)</term>
<term>Fibrosarcoma (metabolism)</term>
<term>Fibrosarcoma (pathology)</term>
<term>Humans</term>
<term>Lymphatic Vessels (metabolism)</term>
<term>Lymphatic Vessels (pathology)</term>
<term>Mice</term>
<term>Mice, Nude</term>
<term>Mitogen-Activated Protein Kinase 1 (genetics)</term>
<term>Mitogen-Activated Protein Kinase 1 (metabolism)</term>
<term>Mitogen-Activated Protein Kinase 3 (genetics)</term>
<term>Mitogen-Activated Protein Kinase 3 (metabolism)</term>
<term>Neoplasms, Experimental (genetics)</term>
<term>Neoplasms, Experimental (metabolism)</term>
<term>Neoplasms, Experimental (pathology)</term>
<term>Neovascularization, Pathologic (genetics)</term>
<term>Neovascularization, Pathologic (metabolism)</term>
<term>Neovascularization, Pathologic (pathology)</term>
<term>Vascular Endothelial Growth Factor C (genetics)</term>
<term>Vascular Endothelial Growth Factor C (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Angiopoïétines (génétique)</term>
<term>Angiopoïétines (métabolisme)</term>
<term>Animaux</term>
<term>Cellules endothéliales (anatomopathologie)</term>
<term>Cellules endothéliales (métabolisme)</term>
<term>Facteur de croissance endothéliale vasculaire de type C (génétique)</term>
<term>Facteur de croissance endothéliale vasculaire de type C (métabolisme)</term>
<term>Fibrosarcome (anatomopathologie)</term>
<term>Fibrosarcome (génétique)</term>
<term>Fibrosarcome (métabolisme)</term>
<term>Humains</term>
<term>Mitogen-Activated Protein Kinase 1 (génétique)</term>
<term>Mitogen-Activated Protein Kinase 1 (métabolisme)</term>
<term>Mitogen-Activated Protein Kinase 3 (génétique)</term>
<term>Mitogen-Activated Protein Kinase 3 (métabolisme)</term>
<term>Néovascularisation pathologique (anatomopathologie)</term>
<term>Néovascularisation pathologique (génétique)</term>
<term>Néovascularisation pathologique (métabolisme)</term>
<term>Perméabilité capillaire</term>
<term>Souris</term>
<term>Souris nude</term>
<term>Tumeurs expérimentales (anatomopathologie)</term>
<term>Tumeurs expérimentales (génétique)</term>
<term>Tumeurs expérimentales (métabolisme)</term>
<term>Vaisseaux lymphatiques (anatomopathologie)</term>
<term>Vaisseaux lymphatiques (métabolisme)</term>
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<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Angiopoietins</term>
<term>Mitogen-Activated Protein Kinase 1</term>
<term>Mitogen-Activated Protein Kinase 3</term>
<term>Vascular Endothelial Growth Factor C</term>
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<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Angiopoietins</term>
<term>Mitogen-Activated Protein Kinase 1</term>
<term>Mitogen-Activated Protein Kinase 3</term>
<term>Vascular Endothelial Growth Factor C</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Cellules endothéliales</term>
<term>Fibrosarcome</term>
<term>Néovascularisation pathologique</term>
<term>Tumeurs expérimentales</term>
<term>Vaisseaux lymphatiques</term>
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<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Fibrosarcoma</term>
<term>Neoplasms, Experimental</term>
<term>Neovascularization, Pathologic</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Angiopoïétines</term>
<term>Facteur de croissance endothéliale vasculaire de type C</term>
<term>Fibrosarcome</term>
<term>Mitogen-Activated Protein Kinase 1</term>
<term>Mitogen-Activated Protein Kinase 3</term>
<term>Néovascularisation pathologique</term>
<term>Tumeurs expérimentales</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Endothelial Cells</term>
<term>Fibrosarcoma</term>
<term>Lymphatic Vessels</term>
<term>Neoplasms, Experimental</term>
<term>Neovascularization, Pathologic</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Angiopoïétines</term>
<term>Cellules endothéliales</term>
<term>Facteur de croissance endothéliale vasculaire de type C</term>
<term>Fibrosarcome</term>
<term>Mitogen-Activated Protein Kinase 1</term>
<term>Mitogen-Activated Protein Kinase 3</term>
<term>Néovascularisation pathologique</term>
<term>Tumeurs expérimentales</term>
<term>Vaisseaux lymphatiques</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Endothelial Cells</term>
<term>Fibrosarcoma</term>
<term>Lymphatic Vessels</term>
<term>Neoplasms, Experimental</term>
<term>Neovascularization, Pathologic</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Capillary Permeability</term>
<term>Humans</term>
<term>Mice</term>
<term>Mice, Nude</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Humains</term>
<term>Perméabilité capillaire</term>
<term>Souris</term>
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<front><div type="abstract" xml:lang="en"><p>The angiopoietin (Ang) ligands are potential therapeutic targets for lymphatic related diseases, which include lymphedema and cancer. Ang-1 and Ang-2 functions are established, but those of Ang-4 are poorly understood. We used intravital fluorescence microscopy to characterize Ang-4 actions on T241 murine fibrosarcoma-associated vessels in mice. The diameters of lymphatic vessels draining Ang-4- or VEGF-C (positive control)-expressing tumors increased to 123 and 135 μm, respectively, and parental, mock-transduced (negative controls) and tumors expressing Ang-1 or Ang-2 remained at baseline (∼60 μm). Ang-4 decreased human dermal lymphatic endothelial cell (LEC) monolayer permeability by 27% while increasing human dermal blood endothelial cell (BEC) monolayer permeability by 200%. <italic>In vivo</italic>
, Ang-4 stimulated a 4.5-fold increase in tumor-associated blood vessel permeability compared with control when measured using intravital quantitative multiphoton microscopy. Ang-4 activated receptor signaling in both LECs and BECs, evidenced by tyrosine kinase with Ig and endothelial growth factor homology domains-2 (TIE2) receptor, protein kinase B, and Erk1,2 phosphorylation detectable by immunoblotting. These data suggest that Ang-4 actions are mediated through cell-type-specific networks and that lymphatic vessel dilation occurs secondarily to increased vascular leakage. Ang-4 also promoted survival of LECs. Thus, blocking Ang-4 may prune the draining lymphatic vasculature and decrease interstitial fluid pressure (IFP) by reducing vascular permeability.—Kesler, C. T., Pereira, E. R., Cui, C. H., Nelson, G. M., Masuck, D. J., Baish, J. W., Padera, T. P. Angiopoietin-4 increases permeability of blood vessels and promotes lymphatic dilation.</p>
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