Hyaluronidase treatment of acute lymphedema in a mouse tail model.
Identifieur interne : 003589 ( Main/Exploration ); précédent : 003588; suivant : 003590Hyaluronidase treatment of acute lymphedema in a mouse tail model.
Auteurs : H J Jeong ; K H Roh ; G C Kim ; Y O Kim ; J H Lee ; M J Lee ; Y J SimSource :
- Lymphology [ 0024-7766 ] ; 2013.
Descripteurs français
- KwdFr :
- Animaux, Antigènes CD44 (génétique), Antigènes CD44 (métabolisme), Expression des gènes, Facteur de croissance transformant bêta-1 (antagonistes et inhibiteurs), Facteur de croissance transformant bêta-1 (génétique), Facteur de croissance transformant bêta-1 (métabolisme), Facteur de nécrose tumorale alpha (antagonistes et inhibiteurs), Facteur de nécrose tumorale alpha (génétique), Facteur de nécrose tumorale alpha (métabolisme), Femelle, Glycoprotéines (agonistes), Glycoprotéines (génétique), Glycoprotéines (métabolisme), Glycoprotéines membranaires (agonistes), Glycoprotéines membranaires (génétique), Glycoprotéines membranaires (métabolisme), Granulocytes neutrophiles (), Granulocytes neutrophiles (anatomopathologie), Hyaluronoglucosaminidase (administration et posologie), Injections intralésionnelles, Lymphangiogenèse (), Lymphangiogenèse (génétique), Lymphoedème (anatomopathologie), Lymphoedème (génétique), Lymphoedème (métabolisme), Lymphoedème (traitement médicamenteux), Maladie aigüe, Modèles animaux de maladie humaine, Queue, Récepteur-3 au facteur croissance endothéliale vasculaire (agonistes), Récepteur-3 au facteur croissance endothéliale vasculaire (génétique), Récepteur-3 au facteur croissance endothéliale vasculaire (métabolisme), Souris, Vaisseaux lymphatiques (), Vaisseaux lymphatiques (anatomopathologie), Vaisseaux lymphatiques (métabolisme).
- MESH :
- administration et posologie : Hyaluronoglucosaminidase.
- agonistes : Glycoprotéines, Glycoprotéines membranaires, Récepteur-3 au facteur croissance endothéliale vasculaire.
- anatomopathologie : Granulocytes neutrophiles, Lymphoedème, Vaisseaux lymphatiques.
- antagonistes et inhibiteurs : Facteur de croissance transformant bêta-1, Facteur de nécrose tumorale alpha.
- génétique : Antigènes CD44, Facteur de croissance transformant bêta-1, Facteur de nécrose tumorale alpha, Glycoprotéines, Glycoprotéines membranaires, Lymphangiogenèse, Lymphoedème, Récepteur-3 au facteur croissance endothéliale vasculaire.
- métabolisme : Antigènes CD44, Facteur de croissance transformant bêta-1, Facteur de nécrose tumorale alpha, Glycoprotéines, Glycoprotéines membranaires, Lymphoedème, Récepteur-3 au facteur croissance endothéliale vasculaire, Vaisseaux lymphatiques.
- traitement médicamenteux : Lymphoedème.
- Animaux, Expression des gènes, Femelle, Granulocytes neutrophiles, Injections intralésionnelles, Lymphangiogenèse, Maladie aigüe, Modèles animaux de maladie humaine, Queue, Souris, Vaisseaux lymphatiques.
English descriptors
- KwdEn :
- Acute Disease, Animals, Antigens, CD44 (genetics), Antigens, CD44 (metabolism), Disease Models, Animal, Female, Gene Expression, Glycoproteins (agonists), Glycoproteins (genetics), Glycoproteins (metabolism), Hyaluronoglucosaminidase (administration & dosage), Injections, Intralesional, Lymphangiogenesis (drug effects), Lymphangiogenesis (genetics), Lymphatic Vessels (drug effects), Lymphatic Vessels (metabolism), Lymphatic Vessels (pathology), Lymphedema (drug therapy), Lymphedema (genetics), Lymphedema (metabolism), Lymphedema (pathology), Membrane Glycoproteins (agonists), Membrane Glycoproteins (genetics), Membrane Glycoproteins (metabolism), Mice, Neutrophils (drug effects), Neutrophils (pathology), Tail, Transforming Growth Factor beta1 (antagonists & inhibitors), Transforming Growth Factor beta1 (genetics), Transforming Growth Factor beta1 (metabolism), Tumor Necrosis Factor-alpha (antagonists & inhibitors), Tumor Necrosis Factor-alpha (genetics), Tumor Necrosis Factor-alpha (metabolism), Vascular Endothelial Growth Factor Receptor-3 (agonists), Vascular Endothelial Growth Factor Receptor-3 (genetics), Vascular Endothelial Growth Factor Receptor-3 (metabolism).
- MESH :
- chemical , administration & dosage : Hyaluronoglucosaminidase.
- chemical , agonists : Glycoproteins, Membrane Glycoproteins, Vascular Endothelial Growth Factor Receptor-3.
- chemical , antagonists & inhibitors : Transforming Growth Factor beta1, Tumor Necrosis Factor-alpha.
- chemical , genetics : Antigens, CD44, Glycoproteins, Membrane Glycoproteins, Transforming Growth Factor beta1, Tumor Necrosis Factor-alpha, Vascular Endothelial Growth Factor Receptor-3.
- chemical , metabolism : Antigens, CD44, Glycoproteins, Membrane Glycoproteins, Transforming Growth Factor beta1, Tumor Necrosis Factor-alpha, Vascular Endothelial Growth Factor Receptor-3.
- drug effects : Lymphangiogenesis, Lymphatic Vessels, Neutrophils.
- drug therapy : Lymphedema.
- genetics : Lymphangiogenesis, Lymphedema.
- metabolism : Lymphatic Vessels, Lymphedema.
- pathology : Lymphatic Vessels, Lymphedema, Neutrophils.
- Acute Disease, Animals, Disease Models, Animal, Female, Gene Expression, Injections, Intralesional, Mice, Tail.
Abstract
The purpose of this study was to investigate the impact of hyaluronidase (HAase) on lymphedema using an acute mouse tail lymphedema model. Six-week-old mice served to produce acute lymphedema and were then either treated with HAase injection or used as operative controls. An additional group of unmanipulated normal mice was used for comparison. Tail volumes were measured for 23 days and histological changes examined. Western blot analysis was conducted to quantify lymphatic vessel endothelial hyaluronan receptor (LYVE)-1, tumor necrosis factor (TNF)-alpha, transforming growth factor (TGF)-beta1, podoplanin, CD 44, and vascular endothelial growth factor receptor3 (VEGFR3) expression levels. The operative control group showed an increase in thickness of the dermis and subdermis, microlymphatic dilatation, and an increase in neutrophils. In contrast, the HAase treated group exhibited alleviation of inflammation evidenced by a decline in microlymphatic dilatation and neutrophils and an overall increase in microlymphatic vessels. Western blot analysis demonstrated that TNF-alpha and TGF-beta1 expression declined but CD44 expression increased in the HAase treated group. Levels of LYVE1, podoplanin, and VEGFR3 also increased significantly in the HAase group. Our results indicate that HAase treatment in the acute mouse tail model reduced lymphedema volume possibly through degradation of HA trafficking, which reduced inflammation and fibrosis in tissues and stimulated lymphangiogenesis.
PubMed: 25141459
Affiliations:
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xml:lang="en">Hyaluronidase treatment of acute lymphedema in a mouse tail model.</title><author><name sortKey="Jeong, H J" sort="Jeong, H J" uniqKey="Jeong H" first="H J" last="Jeong">H J Jeong</name></author><author><name sortKey="Roh, K H" sort="Roh, K H" uniqKey="Roh K" first="K H" last="Roh">K H Roh</name></author><author><name sortKey="Kim, G C" sort="Kim, G C" uniqKey="Kim G" first="G C" last="Kim">G C Kim</name></author><author><name sortKey="Kim, Y O" sort="Kim, Y O" uniqKey="Kim Y" first="Y O" last="Kim">Y O Kim</name></author><author><name sortKey="Lee, J H" sort="Lee, J H" uniqKey="Lee J" first="J H" last="Lee">J H Lee</name></author><author><name sortKey="Lee, M J" sort="Lee, M J" uniqKey="Lee M" first="M J" last="Lee">M J Lee</name></author><author><name sortKey="Sim, Y J" sort="Sim, Y J" uniqKey="Sim Y" first="Y J" last="Sim">Y J Sim</name></author></analytic><series><title level="j">Lymphology</title><idno type="ISSN">0024-7766</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acute Disease</term><term>Animals</term><term>Antigens, CD44 (genetics)</term><term>Antigens, CD44 (metabolism)</term><term>Disease Models, Animal</term><term>Female</term><term>Gene Expression</term><term>Glycoproteins (agonists)</term><term>Glycoproteins (genetics)</term><term>Glycoproteins (metabolism)</term><term>Hyaluronoglucosaminidase (administration & dosage)</term><term>Injections, Intralesional</term><term>Lymphangiogenesis (drug effects)</term><term>Lymphangiogenesis (genetics)</term><term>Lymphatic Vessels (drug effects)</term><term>Lymphatic Vessels (metabolism)</term><term>Lymphatic Vessels (pathology)</term><term>Lymphedema (drug therapy)</term><term>Lymphedema (genetics)</term><term>Lymphedema (metabolism)</term><term>Lymphedema (pathology)</term><term>Membrane Glycoproteins (agonists)</term><term>Membrane Glycoproteins (genetics)</term><term>Membrane Glycoproteins (metabolism)</term><term>Mice</term><term>Neutrophils (drug effects)</term><term>Neutrophils (pathology)</term><term>Tail</term><term>Transforming Growth Factor beta1 (antagonists & inhibitors)</term><term>Transforming Growth Factor beta1 (genetics)</term><term>Transforming Growth Factor beta1 (metabolism)</term><term>Tumor Necrosis Factor-alpha (antagonists & inhibitors)</term><term>Tumor Necrosis Factor-alpha (genetics)</term><term>Tumor Necrosis Factor-alpha (metabolism)</term><term>Vascular Endothelial Growth Factor Receptor-3 (agonists)</term><term>Vascular Endothelial Growth Factor Receptor-3 (genetics)</term><term>Vascular Endothelial Growth Factor Receptor-3 (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Antigènes CD44 (génétique)</term><term>Antigènes CD44 (métabolisme)</term><term>Expression des gènes</term><term>Facteur de croissance transformant bêta-1 (antagonistes et inhibiteurs)</term><term>Facteur de croissance transformant bêta-1 (génétique)</term><term>Facteur de croissance transformant bêta-1 (métabolisme)</term><term>Facteur de nécrose tumorale alpha (antagonistes et inhibiteurs)</term><term>Facteur de nécrose tumorale alpha (génétique)</term><term>Facteur de nécrose tumorale alpha (métabolisme)</term><term>Femelle</term><term>Glycoprotéines (agonistes)</term><term>Glycoprotéines (génétique)</term><term>Glycoprotéines (métabolisme)</term><term>Glycoprotéines membranaires (agonistes)</term><term>Glycoprotéines membranaires (génétique)</term><term>Glycoprotéines membranaires (métabolisme)</term><term>Granulocytes neutrophiles ()</term><term>Granulocytes neutrophiles (anatomopathologie)</term><term>Hyaluronoglucosaminidase (administration et posologie)</term><term>Injections intralésionnelles</term><term>Lymphangiogenèse ()</term><term>Lymphangiogenèse (génétique)</term><term>Lymphoedème (anatomopathologie)</term><term>Lymphoedème (génétique)</term><term>Lymphoedème (métabolisme)</term><term>Lymphoedème (traitement médicamenteux)</term><term>Maladie aigüe</term><term>Modèles animaux de maladie humaine</term><term>Queue</term><term>Récepteur-3 au facteur croissance endothéliale vasculaire (agonistes)</term><term>Récepteur-3 au facteur croissance endothéliale vasculaire (génétique)</term><term>Récepteur-3 au facteur croissance endothéliale vasculaire (métabolisme)</term><term>Souris</term><term>Vaisseaux lymphatiques ()</term><term>Vaisseaux lymphatiques (anatomopathologie)</term><term>Vaisseaux lymphatiques (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Hyaluronoglucosaminidase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="agonists" xml:lang="en"><term>Glycoproteins</term><term>Membrane Glycoproteins</term><term>Vascular Endothelial Growth Factor Receptor-3</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Transforming Growth Factor beta1</term><term>Tumor Necrosis Factor-alpha</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Antigens, CD44</term><term>Glycoproteins</term><term>Membrane Glycoproteins</term><term>Transforming Growth Factor beta1</term><term>Tumor Necrosis Factor-alpha</term><term>Vascular Endothelial Growth Factor Receptor-3</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Antigens, CD44</term><term>Glycoproteins</term><term>Membrane Glycoproteins</term><term>Transforming Growth Factor beta1</term><term>Tumor Necrosis Factor-alpha</term><term>Vascular Endothelial Growth Factor Receptor-3</term></keywords><keywords scheme="MESH" qualifier="administration et posologie" xml:lang="fr"><term>Hyaluronoglucosaminidase</term></keywords><keywords scheme="MESH" qualifier="agonistes" xml:lang="fr"><term>Glycoprotéines</term><term>Glycoprotéines membranaires</term><term>Récepteur-3 au facteur croissance endothéliale vasculaire</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Granulocytes neutrophiles</term><term>Lymphoedème</term><term>Vaisseaux lymphatiques</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Facteur de croissance transformant bêta-1</term><term>Facteur de nécrose tumorale alpha</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Lymphangiogenesis</term><term>Lymphatic Vessels</term><term>Neutrophils</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Lymphedema</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Lymphangiogenesis</term><term>Lymphedema</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Antigènes CD44</term><term>Facteur de croissance transformant bêta-1</term><term>Facteur de nécrose tumorale alpha</term><term>Glycoprotéines</term><term>Glycoprotéines membranaires</term><term>Lymphangiogenèse</term><term>Lymphoedème</term><term>Récepteur-3 au facteur croissance endothéliale vasculaire</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Lymphatic Vessels</term><term>Lymphedema</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Antigènes CD44</term><term>Facteur de croissance transformant bêta-1</term><term>Facteur de nécrose tumorale alpha</term><term>Glycoprotéines</term><term>Glycoprotéines membranaires</term><term>Lymphoedème</term><term>Récepteur-3 au facteur croissance endothéliale vasculaire</term><term>Vaisseaux lymphatiques</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lymphatic Vessels</term><term>Lymphedema</term><term>Neutrophils</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Lymphoedème</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Acute Disease</term><term>Animals</term><term>Disease Models, Animal</term><term>Female</term><term>Gene Expression</term><term>Injections, Intralesional</term><term>Mice</term><term>Tail</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Expression des gènes</term><term>Femelle</term><term>Granulocytes neutrophiles</term><term>Injections intralésionnelles</term><term>Lymphangiogenèse</term><term>Maladie aigüe</term><term>Modèles animaux de maladie humaine</term><term>Queue</term><term>Souris</term><term>Vaisseaux lymphatiques</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The purpose of this study was to investigate the impact of hyaluronidase (HAase) on lymphedema using an acute mouse tail lymphedema model. Six-week-old mice served to produce acute lymphedema and were then either treated with HAase injection or used as operative controls. An additional group of unmanipulated normal mice was used for comparison. Tail volumes were measured for 23 days and histological changes examined. Western blot analysis was conducted to quantify lymphatic vessel endothelial hyaluronan receptor (LYVE)-1, tumor necrosis factor (TNF)-alpha, transforming growth factor (TGF)-beta1, podoplanin, CD 44, and vascular endothelial growth factor receptor3 (VEGFR3) expression levels. The operative control group showed an increase in thickness of the dermis and subdermis, microlymphatic dilatation, and an increase in neutrophils. In contrast, the HAase treated group exhibited alleviation of inflammation evidenced by a decline in microlymphatic dilatation and neutrophils and an overall increase in microlymphatic vessels. Western blot analysis demonstrated that TNF-alpha and TGF-beta1 expression declined but CD44 expression increased in the HAase treated group. Levels of LYVE1, podoplanin, and VEGFR3 also increased significantly in the HAase group. Our results indicate that HAase treatment in the acute mouse tail model reduced lymphedema volume possibly through degradation of HA trafficking, which reduced inflammation and fibrosis in tissues and stimulated lymphangiogenesis.</div></front></TEI><affiliations><list></list><tree><noCountry><name sortKey="Jeong, H J" sort="Jeong, H J" uniqKey="Jeong H" first="H J" last="Jeong">H J Jeong</name><name sortKey="Kim, G C" sort="Kim, G C" uniqKey="Kim G" first="G C" last="Kim">G C Kim</name><name sortKey="Kim, Y O" sort="Kim, Y O" uniqKey="Kim Y" first="Y O" last="Kim">Y O Kim</name><name sortKey="Lee, J H" sort="Lee, J H" uniqKey="Lee J" first="J H" last="Lee">J H Lee</name><name sortKey="Lee, M J" sort="Lee, M J" uniqKey="Lee M" first="M J" last="Lee">M J Lee</name><name sortKey="Roh, K H" sort="Roh, K H" uniqKey="Roh K" first="K H" last="Roh">K H Roh</name><name sortKey="Sim, Y J" sort="Sim, Y J" uniqKey="Sim Y" first="Y J" last="Sim">Y J Sim</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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