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
Links to Exploration step
pubmed:25977256Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Angiopoietin-4 increases permeability of blood vessels and promotes lymphatic dilation.</title><author><name sortKey="Kesler, Cristina T" sort="Kesler, Cristina T" uniqKey="Kesler C" first="Cristina T" last="Kesler">Cristina T. Kesler</name><affiliation><nlm:affiliation>*Edwin Steele Laboratory for Tumor Biology, Department of Radiation Oncology, Massachusetts General Hospital, Boston, Massachusetts, USA; Harold B. Lee Library, Brigham Young University, Provo, Utah, USA; and Department of Biomedical Engineering, Bucknell University, Lewisburg, Pennsylvania, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Pereira, Ethel R" sort="Pereira, Ethel R" uniqKey="Pereira E" first="Ethel R" last="Pereira">Ethel R. Pereira</name><affiliation><nlm:affiliation>*Edwin Steele Laboratory for Tumor Biology, Department of Radiation Oncology, Massachusetts General Hospital, Boston, Massachusetts, USA; Harold B. Lee Library, Brigham Young University, Provo, Utah, USA; and Department of Biomedical Engineering, Bucknell University, Lewisburg, Pennsylvania, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Cui, Cheryl H" sort="Cui, Cheryl H" uniqKey="Cui C" first="Cheryl H" last="Cui">Cheryl H. Cui</name><affiliation><nlm:affiliation>*Edwin Steele Laboratory for Tumor Biology, Department of Radiation Oncology, Massachusetts General Hospital, Boston, Massachusetts, USA; Harold B. Lee Library, Brigham Young University, Provo, Utah, USA; and Department of Biomedical Engineering, Bucknell University, Lewisburg, Pennsylvania, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Nelson, Gregory M" sort="Nelson, Gregory M" uniqKey="Nelson G" first="Gregory M" last="Nelson">Gregory M. 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Lee Library, Brigham Young University, Provo, Utah, USA; and Department of Biomedical Engineering, Bucknell University, Lewisburg, Pennsylvania, USA tpadera@steele.mgh.harvard.edu.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2015">2015</date><idno type="RBID">pubmed:25977256</idno><idno type="pmid">25977256</idno><idno type="doi">10.1096/fj.14-268920</idno><idno type="wicri:Area/PubMed/Corpus">000E91</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000E91</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Angiopoietin-4 increases permeability of blood vessels and promotes lymphatic dilation.</title><author><name sortKey="Kesler, Cristina T" sort="Kesler, Cristina T" uniqKey="Kesler C" first="Cristina T" last="Kesler">Cristina T. Kesler</name><affiliation><nlm:affiliation>*Edwin Steele Laboratory for Tumor Biology, Department of Radiation Oncology, Massachusetts General Hospital, Boston, Massachusetts, USA; Harold B. Lee Library, Brigham Young University, Provo, Utah, USA; and Department of Biomedical Engineering, Bucknell University, Lewisburg, Pennsylvania, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Pereira, Ethel R" sort="Pereira, Ethel R" uniqKey="Pereira E" first="Ethel R" last="Pereira">Ethel R. Pereira</name><affiliation><nlm:affiliation>*Edwin Steele Laboratory for Tumor Biology, Department of Radiation Oncology, Massachusetts General Hospital, Boston, Massachusetts, USA; Harold B. Lee Library, Brigham Young University, Provo, Utah, USA; and Department of Biomedical Engineering, Bucknell University, Lewisburg, Pennsylvania, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Cui, Cheryl H" sort="Cui, Cheryl H" uniqKey="Cui C" first="Cheryl H" last="Cui">Cheryl H. Cui</name><affiliation><nlm:affiliation>*Edwin Steele Laboratory for Tumor Biology, Department of Radiation Oncology, Massachusetts General Hospital, Boston, Massachusetts, USA; Harold B. Lee Library, Brigham Young University, Provo, Utah, USA; and Department of Biomedical Engineering, Bucknell University, Lewisburg, Pennsylvania, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Nelson, Gregory M" sort="Nelson, Gregory M" uniqKey="Nelson G" first="Gregory M" last="Nelson">Gregory M. Nelson</name><affiliation><nlm:affiliation>*Edwin Steele Laboratory for Tumor Biology, Department of Radiation Oncology, Massachusetts General Hospital, Boston, Massachusetts, USA; Harold B. Lee Library, Brigham Young University, Provo, Utah, USA; and Department of Biomedical Engineering, Bucknell University, Lewisburg, Pennsylvania, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Masuck, David J" sort="Masuck, David J" uniqKey="Masuck D" first="David J" last="Masuck">David J. Masuck</name><affiliation><nlm:affiliation>*Edwin Steele Laboratory for Tumor Biology, Department of Radiation Oncology, Massachusetts General Hospital, Boston, Massachusetts, USA; Harold B. Lee Library, Brigham Young University, Provo, Utah, USA; and Department of Biomedical Engineering, Bucknell University, Lewisburg, Pennsylvania, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Baish, James W" sort="Baish, James W" uniqKey="Baish J" first="James W" last="Baish">James W. Baish</name><affiliation><nlm:affiliation>*Edwin Steele Laboratory for Tumor Biology, Department of Radiation Oncology, Massachusetts General Hospital, Boston, Massachusetts, USA; Harold B. Lee Library, Brigham Young University, Provo, Utah, USA; and Department of Biomedical Engineering, Bucknell University, Lewisburg, Pennsylvania, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Padera, Timothy P" sort="Padera, Timothy P" uniqKey="Padera T" first="Timothy P" last="Padera">Timothy P. Padera</name><affiliation><nlm:affiliation>*Edwin Steele Laboratory for Tumor Biology, Department of Radiation Oncology, Massachusetts General Hospital, Boston, Massachusetts, USA; Harold B. Lee Library, Brigham Young University, Provo, Utah, USA; and Department of Biomedical Engineering, Bucknell University, Lewisburg, Pennsylvania, USA tpadera@steele.mgh.harvard.edu.</nlm:affiliation></affiliation></author></analytic><series><title level="j">FASEB journal : official publication of the Federation of American Societies for Experimental Biology</title><idno type="eISSN">1530-6860</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><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="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></keywords></textClass></profileDesc></teiHeader><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></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25977256</PMID><DateCreated><Year>2015</Year><Month>09</Month><Day>02</Day></DateCreated><DateCompleted><Year>2015</Year><Month>11</Month><Day>25</Day></DateCompleted><DateRevised><Year>2016</Year><Month>12</Month><Day>02</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1530-6860</ISSN><JournalIssue CitedMedium="Internet"><Volume>29</Volume><Issue>9</Issue><PubDate><Year>2015</Year><Month>Sep</Month></PubDate></JournalIssue><Title>FASEB journal : official publication of the Federation of American Societies for Experimental Biology</Title><ISOAbbreviation>FASEB J.</ISOAbbreviation></Journal><ArticleTitle>Angiopoietin-4 increases permeability of blood vessels and promotes lymphatic dilation.</ArticleTitle><Pagination><MedlinePgn>3668-77</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1096/fj.14-268920</ELocationID><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><CopyrightInformation>© FASEB.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kesler</LastName><ForeName>Cristina T</ForeName><Initials>CT</Initials><AffiliationInfo><Affiliation>*Edwin Steele Laboratory for Tumor Biology, Department of Radiation Oncology, Massachusetts General Hospital, Boston, Massachusetts, USA; Harold B. Lee Library, Brigham Young University, Provo, Utah, USA; and Department of Biomedical Engineering, Bucknell University, Lewisburg, Pennsylvania, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pereira</LastName><ForeName>Ethel R</ForeName><Initials>ER</Initials><AffiliationInfo><Affiliation>*Edwin Steele Laboratory for Tumor Biology, Department of Radiation Oncology, Massachusetts General Hospital, Boston, Massachusetts, USA; Harold B. Lee Library, Brigham Young University, Provo, Utah, USA; and Department of Biomedical Engineering, Bucknell University, Lewisburg, Pennsylvania, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cui</LastName><ForeName>Cheryl H</ForeName><Initials>CH</Initials><AffiliationInfo><Affiliation>*Edwin Steele Laboratory for Tumor Biology, Department of Radiation Oncology, Massachusetts General Hospital, Boston, Massachusetts, USA; Harold B. Lee Library, Brigham Young University, Provo, Utah, USA; and Department of Biomedical Engineering, Bucknell University, Lewisburg, Pennsylvania, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nelson</LastName><ForeName>Gregory M</ForeName><Initials>GM</Initials><AffiliationInfo><Affiliation>*Edwin Steele Laboratory for Tumor Biology, Department of Radiation Oncology, Massachusetts General Hospital, Boston, Massachusetts, USA; Harold B. Lee Library, Brigham Young University, Provo, Utah, USA; and Department of Biomedical Engineering, Bucknell University, Lewisburg, Pennsylvania, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Masuck</LastName><ForeName>David J</ForeName><Initials>DJ</Initials><AffiliationInfo><Affiliation>*Edwin Steele Laboratory for Tumor Biology, Department of Radiation Oncology, Massachusetts General Hospital, Boston, Massachusetts, USA; Harold B. Lee Library, Brigham Young University, Provo, Utah, USA; and Department of Biomedical Engineering, Bucknell University, Lewisburg, Pennsylvania, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Baish</LastName><ForeName>James W</ForeName><Initials>JW</Initials><AffiliationInfo><Affiliation>*Edwin Steele Laboratory for Tumor Biology, Department of Radiation Oncology, Massachusetts General Hospital, Boston, Massachusetts, USA; Harold B. Lee Library, Brigham Young University, Provo, Utah, USA; and Department of Biomedical Engineering, Bucknell University, Lewisburg, Pennsylvania, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Padera</LastName><ForeName>Timothy P</ForeName><Initials>TP</Initials><AffiliationInfo><Affiliation>*Edwin Steele Laboratory for Tumor Biology, Department of Radiation Oncology, Massachusetts General Hospital, Boston, Massachusetts, USA; Harold B. Lee Library, Brigham Young University, Provo, Utah, USA; and Department of Biomedical Engineering, Bucknell University, Lewisburg, Pennsylvania, USA tpadera@steele.mgh.harvard.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R00CA137167</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R00 CA137167</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>C06 CA059267</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>DP2OD008780</GrantID><Acronym>OD</Acronym><Agency>NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>DP2 OD008780</GrantID><Acronym>OD</Acronym><Agency>NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>05</Month><Day>14</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>FASEB J</MedlineTA><NlmUniqueID>8804484</NlmUniqueID><ISSNLinking>0892-6638</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D042682">Angiopoietins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C495961">Angpt4 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C467486">VEGFC protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D042582">Vascular Endothelial Growth Factor C</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C467483">vascular endothelial growth factor C, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.24</RegistryNumber><NameOfSubstance UI="C535150">MAPK1 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.24</RegistryNumber><NameOfSubstance UI="D019950">Mitogen-Activated Protein Kinase 1</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.24</RegistryNumber><NameOfSubstance UI="D048052">Mitogen-Activated Protein Kinase 3</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Cancer Cell. 2012 Feb 14;21(2):181-95</RefSource><PMID Version="1">22340592</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Dev Cell. 2002 Sep;3(3):411-23</RefSource><PMID Version="1">12361603</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Natl Cancer Inst. 2013 Aug 21;105(16):1188-201</RefSource><PMID 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Chem. 2001 Jul 13;276(28):26516-25</RefSource><PMID Version="1">11346644</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Science. 2002 Jun 7;296(5574):1883-6</RefSource><PMID Version="1">11976409</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2002 Aug 20;99(17):11205-10</RefSource><PMID Version="1">12163646</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Am J Pathol. 2012 Jun;180(6):2561-75</RefSource><PMID Version="1">22538088</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D042682" MajorTopicYN="N">Angiopoietins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002199" MajorTopicYN="Y">Capillary Permeability</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D042783" MajorTopicYN="N">Endothelial Cells</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005354" MajorTopicYN="N">Fibrosarcoma</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D042601" MajorTopicYN="N">Lymphatic Vessels</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008819" MajorTopicYN="N">Mice, Nude</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019950" MajorTopicYN="N">Mitogen-Activated Protein Kinase 1</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D048052" MajorTopicYN="N">Mitogen-Activated Protein Kinase 3</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009374" MajorTopicYN="N">Neoplasms, Experimental</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009389" MajorTopicYN="N">Neovascularization, Pathologic</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D042582" MajorTopicYN="N">Vascular Endothelial Growth Factor C</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">PMC4550378</OtherID><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">2-photon microscopy</Keyword><Keyword MajorTopicYN="N">TIE2</Keyword><Keyword MajorTopicYN="N">endothelial</Keyword><Keyword MajorTopicYN="N">lymphangiography</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2014</Year><Month>12</Month><Day>18</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2015</Year><Month>05</Month><Day>04</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>5</Month><Day>16</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>5</Month><Day>16</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>12</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">25977256</ArticleId><ArticleId IdType="pii">fj.14-268920</ArticleId><ArticleId IdType="doi">10.1096/fj.14-268920</ArticleId><ArticleId IdType="pmc">PMC4550378</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour 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