Lymphatic function is regulated by a coordinated expression of lymphangiogenic and anti-lymphangiogenic cytokines
Identifieur interne : 004688 ( Ncbi/Curation ); précédent : 004687; suivant : 004689Lymphatic function is regulated by a coordinated expression of lymphangiogenic and anti-lymphangiogenic cytokines
Auteurs : Jamie C. Zampell ; Tomer Avraham ; Nicole Yoder ; Nicholas Fort ; Alan Yan ; Evan S. Weitman ; Babak J. MehraraSource :
- American Journal of Physiology - Cell Physiology [ 0363-6143 ] ; 2011.
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.
Url:
DOI: 10.1152/ajpcell.00306.2011
PubMed: 21940662
PubMed Central: 3328842
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PMC:3328842Le document en format XML
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Mehrara</name></author></analytic><series><title level="j">American Journal of Physiology - Cell Physiology</title><idno type="ISSN">0363-6143</idno><idno type="eISSN">1522-1563</idno><imprint><date when="2011">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Cytokines (metabolism)</term><term>Female</term><term>Hepatocyte Growth Factor (metabolism)</term><term>Inflammation (metabolism)</term><term>Inflammation (pathology)</term><term>Interferon-gamma (antagonists & inhibitors)</term><term>Interferon-gamma (metabolism)</term><term>Lymph (metabolism)</term><term>Lymphangiogenesis (physiology)</term><term>Lymphatic System (pathology)</term><term>Lymphatic System (physiology)</term><term>Lymphatic System (physiopathology)</term><term>Lymphedema (metabolism)</term><term>Lymphedema (pathology)</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Nude</term><term>Regeneration (physiology)</term><term>T-Lymphocytes (immunology)</term><term>Tail (anatomy & histology)</term><term>Tail (metabolism)</term><term>Tail (pathology)</term><term>Tail (physiopathology)</term><term>Vascular Endothelial Growth Factor A (metabolism)</term><term>Vascular Endothelial Growth Factor C (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Cytokines (métabolisme)</term><term>Facteur de croissance des hépatocytes (métabolisme)</term><term>Facteur de croissance endothéliale vasculaire de type A (métabolisme)</term><term>Facteur de croissance endothéliale vasculaire de type C (métabolisme)</term><term>Femelle</term><term>Inflammation (anatomopathologie)</term><term>Inflammation (métabolisme)</term><term>Interféron gamma (antagonistes et inhibiteurs)</term><term>Interféron gamma (métabolisme)</term><term>Lymphangiogenèse (physiologie)</term><term>Lymphe (métabolisme)</term><term>Lymphocytes T 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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"><p>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.</p></div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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