Lymphatic function is regulated by a coordinated expression of lymphangiogenic and anti-lymphangiogenic cytokines.
Identifieur interne : 002456 ( PubMed/Curation ); précédent : 002455; suivant : 002457Lymphatic function is regulated by a coordinated expression of lymphangiogenic and anti-lymphangiogenic cytokines.
Auteurs : Jamie C. Zampell [États-Unis] ; Tomer Avraham ; Nicole Yoder ; Nicholas Fort ; Alan Yan ; Evan S. Weitman ; Babak J. MehraraSource :
- American journal of physiology. Cell physiology [ 1522-1563 ] ; 2012.
Descripteurs français
- KwdFr :
- Animaux, Cytokines (métabolisme), Facteur de croissance des hépatocytes (métabolisme), Facteur de croissance endothéliale vasculaire de type A (métabolisme), Facteur de croissance endothéliale vasculaire de type C (métabolisme), Femelle, Inflammation (anatomopathologie), Inflammation (métabolisme), Interféron gamma (antagonistes et inhibiteurs), Interféron gamma (métabolisme), Lymphangiogenèse (physiologie), Lymphe (métabolisme), Lymphocytes T (immunologie), Lymphoedème (anatomopathologie), Lymphoedème (métabolisme), Queue (anatomie et histologie), Queue (anatomopathologie), Queue (métabolisme), Queue (physiopathologie), Régénération (physiologie), Souris, Souris de lignée C57BL, Souris nude, Système lymphatique (anatomopathologie), Système lymphatique (physiologie), Système lymphatique (physiopathologie).
- MESH :
- anatomie et histologie : Queue.
- anatomopathologie : Inflammation, Lymphoedème, Queue, Système lymphatique.
- antagonistes et inhibiteurs : Interféron gamma.
- immunologie : Lymphocytes T.
- métabolisme : Cytokines, Facteur de croissance des hépatocytes, Facteur de croissance endothéliale vasculaire de type A, Facteur de croissance endothéliale vasculaire de type C, Inflammation, Interféron gamma, Lymphe, Lymphoedème, Queue.
- physiologie : Lymphangiogenèse, Régénération, Système lymphatique.
- physiopathologie : Queue, Système lymphatique.
- Animaux, Femelle, Souris, Souris de lignée C57BL, Souris nude.
English descriptors
- KwdEn :
- Animals, Cytokines (metabolism), Female, Hepatocyte Growth Factor (metabolism), Inflammation (metabolism), Inflammation (pathology), Interferon-gamma (antagonists & inhibitors), Interferon-gamma (metabolism), Lymph (metabolism), Lymphangiogenesis (physiology), Lymphatic System (pathology), Lymphatic System (physiology), Lymphatic System (physiopathology), Lymphedema (metabolism), Lymphedema (pathology), Mice, Mice, Inbred C57BL, Mice, Nude, Regeneration (physiology), T-Lymphocytes (immunology), Tail (anatomy & histology), Tail (metabolism), Tail (pathology), Tail (physiopathology), Vascular Endothelial Growth Factor A (metabolism), Vascular Endothelial Growth Factor C (metabolism).
- MESH :
- chemical , antagonists & inhibitors : Interferon-gamma.
- chemical , metabolism : Cytokines, Hepatocyte Growth Factor, Interferon-gamma, Vascular Endothelial Growth Factor A, Vascular Endothelial Growth Factor C.
- anatomy & histology : Tail.
- immunology : T-Lymphocytes.
- metabolism : Inflammation, Lymph, Lymphedema, Tail.
- pathology : Inflammation, Lymphatic System, Lymphedema, Tail.
- physiology : Lymphangiogenesis, Lymphatic System, Regeneration.
- physiopathology : Lymphatic System, Tail.
- Animals, Female, Mice, Mice, Inbred C57BL, Mice, Nude.
Abstract
Lymphangiogenic cytokines such as vascular endothelial growth factor-C (VEGF-C) are critically required for lymphatic regeneration; however, in some circumstances, lymphatic function is impaired despite normal or elevated levels of these cytokines. The recent identification of anti-lymphangiogenic molecules such as interferon-γ (IFN-γ), transforming growth factor-β1, and endostatin has led us to hypothesize that impaired lymphatic function may represent a dysregulated balance in the expression of pro/anti-lymphangiogenic stimuli. We observed that nude mice have significantly improved lymphatic function compared with wild-type mice in a tail model of lymphedema. We show that gradients of lymphatic fluid stasis regulate the expression of lymphangiogenic cytokines (VEGF-A, VEGF-C, and hepatocyte growth factor) and that paradoxically the expression of these molecules is increased in wild-type mice. More importantly, we show that as a consequence of T-cell-mediated inflammation, these same gradients also regulate expression patterns of anti-lymphangiogenic molecules corresponding temporally and spatially with impaired lymphatic function in wild-type mice. We show that neutralization of IFN-γ significantly increases inflammatory lymph node lymphangiogenesis independently of changes in VEGF-A or VEGF-C expression, suggesting that alterations in the balance of pro- and anti-lymphangiogenic cytokine expression can regulate lymphatic vessel formation. In conclusion, we show that gradients of lymphatic fluid stasis regulate not only the expression of pro-lymphangiogenic cytokines but also potent suppressors of lymphangiogenesis as a consequence of T-cell inflammation and that modulation of the balance between these stimuli can regulate lymphatic function.
DOI: 10.1152/ajpcell.00306.2011
PubMed: 21940662
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Zampell</name><affiliation wicri:level="1"><nlm:affiliation>The Division of Plastic and Reconstructive Surgery, Department of Surgery, Memorial Sloan-Kettering Cancer Center, New York, New York, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>The Division of Plastic and Reconstructive Surgery, Department of Surgery, Memorial Sloan-Kettering Cancer Center, New York, New York</wicri:regionArea></affiliation></author><author><name sortKey="Avraham, Tomer" sort="Avraham, Tomer" uniqKey="Avraham T" first="Tomer" last="Avraham">Tomer Avraham</name></author><author><name sortKey="Yoder, Nicole" sort="Yoder, Nicole" uniqKey="Yoder N" first="Nicole" last="Yoder">Nicole Yoder</name></author><author><name sortKey="Fort, Nicholas" sort="Fort, Nicholas" uniqKey="Fort N" first="Nicholas" last="Fort">Nicholas Fort</name></author><author><name sortKey="Yan, Alan" sort="Yan, Alan" uniqKey="Yan A" first="Alan" last="Yan">Alan Yan</name></author><author><name sortKey="Weitman, Evan S" sort="Weitman, Evan S" uniqKey="Weitman E" first="Evan S" last="Weitman">Evan S. 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histologie)</term><term>Queue (anatomopathologie)</term><term>Queue (métabolisme)</term><term>Queue (physiopathologie)</term><term>Régénération (physiologie)</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Souris nude</term><term>Système lymphatique (anatomopathologie)</term><term>Système lymphatique (physiologie)</term><term>Système lymphatique (physiopathologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Interferon-gamma</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cytokines</term><term>Hepatocyte Growth Factor</term><term>Interferon-gamma</term><term>Vascular Endothelial Growth Factor A</term><term>Vascular Endothelial Growth Factor C</term></keywords><keywords scheme="MESH" qualifier="anatomie et histologie" xml:lang="fr"><term>Queue</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Inflammation</term><term>Lymphoedème</term><term>Queue</term><term>Système lymphatique</term></keywords><keywords scheme="MESH" qualifier="anatomy & histology" xml:lang="en"><term>Tail</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Interféron gamma</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Lymphocytes T</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>T-Lymphocytes</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Inflammation</term><term>Lymph</term><term>Lymphedema</term><term>Tail</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cytokines</term><term>Facteur de croissance des hépatocytes</term><term>Facteur de croissance endothéliale vasculaire de type A</term><term>Facteur de croissance endothéliale vasculaire de type C</term><term>Inflammation</term><term>Interféron gamma</term><term>Lymphe</term><term>Lymphoedème</term><term>Queue</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Inflammation</term><term>Lymphatic System</term><term>Lymphedema</term><term>Tail</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Lymphangiogenèse</term><term>Régénération</term><term>Système lymphatique</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Lymphangiogenesis</term><term>Lymphatic System</term><term>Regeneration</term></keywords><keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Queue</term><term>Système lymphatique</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Lymphatic System</term><term>Tail</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Female</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Nude</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Femelle</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Souris nude</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Lymphangiogenic cytokines such as vascular endothelial growth factor-C (VEGF-C) are critically required for lymphatic regeneration; however, in some circumstances, lymphatic function is impaired despite normal or elevated levels of these cytokines. The recent identification of anti-lymphangiogenic molecules such as interferon-γ (IFN-γ), transforming growth factor-β1, and endostatin has led us to hypothesize that impaired lymphatic function may represent a dysregulated balance in the expression of pro/anti-lymphangiogenic stimuli. We observed that nude mice have significantly improved lymphatic function compared with wild-type mice in a tail model of lymphedema. We show that gradients of lymphatic fluid stasis regulate the expression of lymphangiogenic cytokines (VEGF-A, VEGF-C, and hepatocyte growth factor) and that paradoxically the expression of these molecules is increased in wild-type mice. More importantly, we show that as a consequence of T-cell-mediated inflammation, these same gradients also regulate expression patterns of anti-lymphangiogenic molecules corresponding temporally and spatially with impaired lymphatic function in wild-type mice. We show that neutralization of IFN-γ significantly increases inflammatory lymph node lymphangiogenesis independently of changes in VEGF-A or VEGF-C expression, suggesting that alterations in the balance of pro- and anti-lymphangiogenic cytokine expression can regulate lymphatic vessel formation. In conclusion, we show that gradients of lymphatic fluid stasis regulate not only the expression of pro-lymphangiogenic cytokines but also potent suppressors of lymphangiogenesis as a consequence of T-cell inflammation and that modulation of the balance between these stimuli can regulate lymphatic function.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">21940662</PMID><DateCreated><Year>2012</Year><Month>01</Month><Day>04</Day></DateCreated><DateCompleted><Year>2012</Year><Month>03</Month><Day>08</Day></DateCompleted><DateRevised><Year>2016</Year><Month>10</Month><Day>25</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1522-1563</ISSN><JournalIssue CitedMedium="Internet"><Volume>302</Volume><Issue>2</Issue><PubDate><Year>2012</Year><Month>Jan</Month><Day>15</Day></PubDate></JournalIssue><Title>American journal of physiology. Cell physiology</Title><ISOAbbreviation>Am. J. Physiol., Cell Physiol.</ISOAbbreviation></Journal><ArticleTitle>Lymphatic function is regulated by a coordinated expression of lymphangiogenic and anti-lymphangiogenic cytokines.</ArticleTitle><Pagination><MedlinePgn>C392-404</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1152/ajpcell.00306.2011</ELocationID><Abstract><AbstractText>Lymphangiogenic cytokines such as vascular endothelial growth factor-C (VEGF-C) are critically required for lymphatic regeneration; however, in some circumstances, lymphatic function is impaired despite normal or elevated levels of these cytokines. The recent identification of anti-lymphangiogenic molecules such as interferon-γ (IFN-γ), transforming growth factor-β1, and endostatin has led us to hypothesize that impaired lymphatic function may represent a dysregulated balance in the expression of pro/anti-lymphangiogenic stimuli. We observed that nude mice have significantly improved lymphatic function compared with wild-type mice in a tail model of lymphedema. We show that gradients of lymphatic fluid stasis regulate the expression of lymphangiogenic cytokines (VEGF-A, VEGF-C, and hepatocyte growth factor) and that paradoxically the expression of these molecules is increased in wild-type mice. More importantly, we show that as a consequence of T-cell-mediated inflammation, these same gradients also regulate expression patterns of anti-lymphangiogenic molecules corresponding temporally and spatially with impaired lymphatic function in wild-type mice. We show that neutralization of IFN-γ significantly increases inflammatory lymph node lymphangiogenesis independently of changes in VEGF-A or VEGF-C expression, suggesting that alterations in the balance of pro- and anti-lymphangiogenic cytokine expression can regulate lymphatic vessel formation. In conclusion, we show that gradients of lymphatic fluid stasis regulate not only the expression of pro-lymphangiogenic cytokines but also potent suppressors of lymphangiogenesis as a consequence of T-cell inflammation and that modulation of the balance between these stimuli can regulate lymphatic function.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zampell</LastName><ForeName>Jamie C</ForeName><Initials>JC</Initials><AffiliationInfo><Affiliation>The Division of Plastic and Reconstructive Surgery, Department of Surgery, Memorial Sloan-Kettering Cancer Center, New York, New York, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Avraham</LastName><ForeName>Tomer</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Yoder</LastName><ForeName>Nicole</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Fort</LastName><ForeName>Nicholas</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Yan</LastName><ForeName>Alan</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Weitman</LastName><ForeName>Evan S</ForeName><Initials>ES</Initials></Author><Author ValidYN="Y"><LastName>Mehrara</LastName><ForeName>Babak J</ForeName><Initials>BJ</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>T32 CA009501</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 CA009501-23</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 CA009501-24</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 CA009501-25</GrantID><Acronym>CA</Acronym><Agency>NCI 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><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2011</Year><Month>09</Month><Day>21</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Am J Physiol Cell Physiol</MedlineTA><NlmUniqueID>100901225</NlmUniqueID><ISSNLinking>0363-6143</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D042461">Vascular Endothelial Growth Factor A</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D042582">Vascular Endothelial Growth Factor C</NameOfSubstance></Chemical><Chemical><RegistryNumber>67256-21-7</RegistryNumber><NameOfSubstance UI="D017228">Hepatocyte Growth Factor</NameOfSubstance></Chemical><Chemical><RegistryNumber>82115-62-6</RegistryNumber><NameOfSubstance UI="D007371">Interferon-gamma</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Cancer. 2001 Sep 15;92(6):1368-77</RefSource><PMID Version="1">11745212</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Breast Cancer Res. 2010;12(5):R70</RefSource><PMID Version="1">20825671</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>FASEB J. 2002 Dec;16(14):1985-7</RefSource><PMID Version="1">12397087</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Clin Invest. 2003 Mar;111(5):717-25</RefSource><PMID Version="1">12618526</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Surgery. 1989 Jun;105(6):764-9</RefSource><PMID Version="1">2567062</PMID></CommentsCorrections><CommentsCorrections 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