Angiopoietin-4 increases permeability of blood vessels and promotes lymphatic dilation.
Identifieur interne : 000E91 ( PubMed/Corpus ); précédent : 000E90; suivant : 000E92Angiopoietin-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 :
- FASEB journal : official publication of the Federation of American Societies for Experimental Biology [ 1530-6860 ] ; 2015.
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%. 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.
DOI: 10.1096/fj.14-268920
PubMed: 25977256
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pubmed:25977256Le document en format XML
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<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="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>
</keywords>
<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="genetics" xml:lang="en"><term>Fibrosarcoma</term>
<term>Neoplasms, Experimental</term>
<term>Neovascularization, Pathologic</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="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>
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<front><div type="abstract" xml:lang="en">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.</div>
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<Abstract><AbstractText>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.</AbstractText>
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<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kesler</LastName>
<ForeName>Cristina T</ForeName>
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