LymphedemaV1, Main, Merge, bibRecord, 002150

Angiopoietin-4 increases permeability of blood vessels and promotes lymphatic dilation

Identifieur interne : 002150 ( Main/Merge ); précédent : 002149; suivant : 002151

Angiopoietin-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. Padera

Source :

The FASEB Journal [ 0892-6638 ] ; 2015.

RBID : PMC:4550378

Descripteurs français

English descriptors

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%. In vivo, 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.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4550378

DOI: 10.1096/fj.14-268920
PubMed: 25977256
PubMed Central: 4550378

Links to Exploration step

PMC:4550378

Le document en format XML

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<author><name sortKey="Pereira, Ethel R" sort="Pereira, Ethel R" uniqKey="Pereira E" first="Ethel R." last="Pereira">Ethel R. Pereira</name>
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<author><name sortKey="Cui, Cheryl H" sort="Cui, Cheryl H" uniqKey="Cui C" first="Cheryl H." last="Cui">Cheryl H. Cui</name>
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<author><name sortKey="Nelson, Gregory M" sort="Nelson, Gregory M" uniqKey="Nelson G" first="Gregory M." last="Nelson">Gregory M. Nelson</name>
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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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<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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<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" 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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<term>Fibrosarcome</term>
<term>Mitogen-Activated Protein Kinase 1</term>
<term>Mitogen-Activated Protein Kinase 3</term>
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<term>Tumeurs expérimentales</term>
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<term>Fibrosarcoma</term>
<term>Lymphatic Vessels</term>
<term>Neoplasms, Experimental</term>
<term>Neovascularization, Pathologic</term>
</keywords>
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<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>
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<term>Lymphatic Vessels</term>
<term>Neoplasms, Experimental</term>
<term>Neovascularization, Pathologic</term>
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<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>
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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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Angiopoietin-4 increases permeability of blood vessels and promotes lymphatic dilation

Angiopoietin-4 increases permeability of blood vessels and promotes lymphatic dilation

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Abstract

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