Secondary lymphedema in the mouse tail: Lymphatic hyperplasia, VEGF-C upregulation, and the protective role of MMP-9.
Identifieur interne : 003511 ( PubMed/Checkpoint ); précédent : 003510; suivant : 003512Secondary lymphedema in the mouse tail: Lymphatic hyperplasia, VEGF-C upregulation, and the protective role of MMP-9.
Auteurs : Joseph M. Rutkowski [Suisse] ; Monica Moya ; Jimmy Johannes ; Jeremy Goldman ; Melody A. SwartzSource :
- Microvascular research [ 0026-2862 ] ; 2006.
Descripteurs français
- KwdFr :
- Animaux, Cellules dendritiques (anatomopathologie), Cellules dendritiques (métabolisme), Cellules endothéliales (anatomopathologie), Cellules endothéliales (métabolisme), Collagène (métabolisme), Derme (anatomopathologie), Derme (métabolisme), Facteur de croissance endothéliale vasculaire de type C (métabolisme), Facteurs temps, Femelle, Hyperplasie, Lignées consanguines de souris, Lymphoedème (anatomopathologie), Lymphoedème (génétique), Lymphoedème (métabolisme), Lymphographie, Macrophages (anatomopathologie), Macrophages (métabolisme), Matrix metalloproteinase 9 (génétique), Modèles animaux de maladie humaine, Mouvement cellulaire, Métabolisme des lipides, Queue (), Queue (anatomopathologie), Queue (métabolisme), Souris, Souris de lignée BALB C, Souris knockout, Tissu sous-cutané (anatomopathologie), Tissu sous-cutané (métabolisme), Vaisseaux lymphatiques (), Vaisseaux lymphatiques (anatomopathologie), Vaisseaux lymphatiques (métabolisme).
- MESH :
- anatomopathologie : Cellules dendritiques, Cellules endothéliales, Derme, Lymphoedème, Macrophages, Queue, Tissu sous-cutané, Vaisseaux lymphatiques.
- génétique : Lymphoedème, Matrix metalloproteinase 9.
- métabolisme : Cellules dendritiques, Cellules endothéliales, Collagène, Derme, Facteur de croissance endothéliale vasculaire de type C, Lymphoedème, Macrophages, Queue, Tissu sous-cutané, Vaisseaux lymphatiques.
- Animaux, Facteurs temps, Femelle, Hyperplasie, Lignées consanguines de souris, Lymphographie, Modèles animaux de maladie humaine, Mouvement cellulaire, Métabolisme des lipides, Queue, Souris, Souris de lignée BALB C, Souris knockout, Vaisseaux lymphatiques.
English descriptors
- KwdEn :
- Animals, Cell Movement, Collagen (metabolism), Dendritic Cells (metabolism), Dendritic Cells (pathology), Dermis (metabolism), Dermis (pathology), Disease Models, Animal, Endothelial Cells (metabolism), Endothelial Cells (pathology), Female, Hyperplasia, Lipid Metabolism, Lymphatic Vessels (metabolism), Lymphatic Vessels (pathology), Lymphatic Vessels (surgery), Lymphedema (genetics), Lymphedema (metabolism), Lymphedema (pathology), Lymphography, Macrophages (metabolism), Macrophages (pathology), Matrix Metalloproteinase 9 (genetics), Mice, Mice, Inbred BALB C, Mice, Inbred Strains, Mice, Knockout, Subcutaneous Tissue (metabolism), Subcutaneous Tissue (pathology), Tail (metabolism), Tail (pathology), Tail (surgery), Time Factors, Vascular Endothelial Growth Factor C (metabolism).
- MESH :
- chemical , genetics : Matrix Metalloproteinase 9.
- chemical , metabolism : Collagen, Vascular Endothelial Growth Factor C.
- genetics : Lymphedema.
- metabolism : Dendritic Cells, Dermis, Endothelial Cells, Lymphatic Vessels, Lymphedema, Macrophages, Subcutaneous Tissue, Tail.
- pathology : Dendritic Cells, Dermis, Endothelial Cells, Lymphatic Vessels, Lymphedema, Macrophages, Subcutaneous Tissue, Tail.
- surgery : Lymphatic Vessels, Tail.
- Animals, Cell Movement, Disease Models, Animal, Female, Hyperplasia, Lipid Metabolism, Lymphography, Mice, Mice, Inbred BALB C, Mice, Inbred Strains, Mice, Knockout, Time Factors.
Abstract
Disturbances in the microcirculation can lead to secondary lymphedema, a common pathological condition that, despite its frequency, still lacks a cure. Lymphedema is clinically well described, but while the genetic underpinnings that cause lymphatic malformations and primary lymphedema are being discovered, the pathophysiology and pathobiology of secondary lymphedema remain poorly understood, partly due to the lack of well-described experimental models. Here, we provide a detailed characterization of secondary lymphedema in the mouse tail and correlate the evolution of tissue swelling to changes in tissue architecture, infiltration of immune cells, deposition of lipids, and proliferation and morphology of the lymphatic vessels. We show that sustained swelling leads to lymphatic hyperplasia and upregulation of vascular endothelial growth factor (VEGF)-C, which may exacerbate the edema because the hyperplastic vessels are poorly functional. The onset of lymphatic hyperplasia occurred prior to the onset of lipid accumulation and peak VEGF-C expression. Langerhans dendritic cells were seen in the dermis migrating from the epidermis to the lymphatic capillaries in edematous tissue. Furthermore, these results were consistent between two different normal mouse strains, but swelling was significantly greater in a matrix metalloproteinase (MMP)-9 null strain. Thus, by characterizing this highly reproducible model of secondary lymphedema, we conclude that VEGF-C upregulation and lymphatic hyperplasia resulting from dermal lymphatic ligation and lymphedema leads to decreased drainage function and that MMP-9 may be important in counteracting tissue swelling.
DOI: 10.1016/j.mvr.2006.05.009
PubMed: 16876204
Affiliations:
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pubmed:16876204Le document en format XML
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<term>Cell Movement</term>
<term>Collagen (metabolism)</term>
<term>Dendritic Cells (metabolism)</term>
<term>Dendritic Cells (pathology)</term>
<term>Dermis (metabolism)</term>
<term>Dermis (pathology)</term>
<term>Disease Models, Animal</term>
<term>Endothelial Cells (metabolism)</term>
<term>Endothelial Cells (pathology)</term>
<term>Female</term>
<term>Hyperplasia</term>
<term>Lipid Metabolism</term>
<term>Lymphatic Vessels (metabolism)</term>
<term>Lymphatic Vessels (pathology)</term>
<term>Lymphatic Vessels (surgery)</term>
<term>Lymphedema (genetics)</term>
<term>Lymphedema (metabolism)</term>
<term>Lymphedema (pathology)</term>
<term>Lymphography</term>
<term>Macrophages (metabolism)</term>
<term>Macrophages (pathology)</term>
<term>Matrix Metalloproteinase 9 (genetics)</term>
<term>Mice</term>
<term>Mice, Inbred BALB C</term>
<term>Mice, Inbred Strains</term>
<term>Mice, Knockout</term>
<term>Subcutaneous Tissue (metabolism)</term>
<term>Subcutaneous Tissue (pathology)</term>
<term>Tail (metabolism)</term>
<term>Tail (pathology)</term>
<term>Tail (surgery)</term>
<term>Time Factors</term>
<term>Vascular Endothelial Growth Factor C (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Cellules dendritiques (anatomopathologie)</term>
<term>Cellules dendritiques (métabolisme)</term>
<term>Cellules endothéliales (anatomopathologie)</term>
<term>Cellules endothéliales (métabolisme)</term>
<term>Collagène (métabolisme)</term>
<term>Derme (anatomopathologie)</term>
<term>Derme (métabolisme)</term>
<term>Facteur de croissance endothéliale vasculaire de type C (métabolisme)</term>
<term>Facteurs temps</term>
<term>Femelle</term>
<term>Hyperplasie</term>
<term>Lignées consanguines de souris</term>
<term>Lymphoedème (anatomopathologie)</term>
<term>Lymphoedème (génétique)</term>
<term>Lymphoedème (métabolisme)</term>
<term>Lymphographie</term>
<term>Macrophages (anatomopathologie)</term>
<term>Macrophages (métabolisme)</term>
<term>Matrix metalloproteinase 9 (génétique)</term>
<term>Modèles animaux de maladie humaine</term>
<term>Mouvement cellulaire</term>
<term>Métabolisme des lipides</term>
<term>Queue ()</term>
<term>Queue (anatomopathologie)</term>
<term>Queue (métabolisme)</term>
<term>Souris</term>
<term>Souris de lignée BALB C</term>
<term>Souris knockout</term>
<term>Tissu sous-cutané (anatomopathologie)</term>
<term>Tissu sous-cutané (métabolisme)</term>
<term>Vaisseaux lymphatiques ()</term>
<term>Vaisseaux lymphatiques (anatomopathologie)</term>
<term>Vaisseaux lymphatiques (métabolisme)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Matrix Metalloproteinase 9</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Collagen</term>
<term>Vascular Endothelial Growth Factor C</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Cellules dendritiques</term>
<term>Cellules endothéliales</term>
<term>Derme</term>
<term>Lymphoedème</term>
<term>Macrophages</term>
<term>Queue</term>
<term>Tissu sous-cutané</term>
<term>Vaisseaux lymphatiques</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Lymphedema</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Lymphoedème</term>
<term>Matrix metalloproteinase 9</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Dendritic Cells</term>
<term>Dermis</term>
<term>Endothelial Cells</term>
<term>Lymphatic Vessels</term>
<term>Lymphedema</term>
<term>Macrophages</term>
<term>Subcutaneous Tissue</term>
<term>Tail</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cellules dendritiques</term>
<term>Cellules endothéliales</term>
<term>Collagène</term>
<term>Derme</term>
<term>Facteur de croissance endothéliale vasculaire de type C</term>
<term>Lymphoedème</term>
<term>Macrophages</term>
<term>Queue</term>
<term>Tissu sous-cutané</term>
<term>Vaisseaux lymphatiques</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Dendritic Cells</term>
<term>Dermis</term>
<term>Endothelial Cells</term>
<term>Lymphatic Vessels</term>
<term>Lymphedema</term>
<term>Macrophages</term>
<term>Subcutaneous Tissue</term>
<term>Tail</term>
</keywords>
<keywords scheme="MESH" qualifier="surgery" xml:lang="en"><term>Lymphatic Vessels</term>
<term>Tail</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Cell Movement</term>
<term>Disease Models, Animal</term>
<term>Female</term>
<term>Hyperplasia</term>
<term>Lipid Metabolism</term>
<term>Lymphography</term>
<term>Mice</term>
<term>Mice, Inbred BALB C</term>
<term>Mice, Inbred Strains</term>
<term>Mice, Knockout</term>
<term>Time Factors</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Facteurs temps</term>
<term>Femelle</term>
<term>Hyperplasie</term>
<term>Lignées consanguines de souris</term>
<term>Lymphographie</term>
<term>Modèles animaux de maladie humaine</term>
<term>Mouvement cellulaire</term>
<term>Métabolisme des lipides</term>
<term>Queue</term>
<term>Souris</term>
<term>Souris de lignée BALB C</term>
<term>Souris knockout</term>
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<front><div type="abstract" xml:lang="en">Disturbances in the microcirculation can lead to secondary lymphedema, a common pathological condition that, despite its frequency, still lacks a cure. Lymphedema is clinically well described, but while the genetic underpinnings that cause lymphatic malformations and primary lymphedema are being discovered, the pathophysiology and pathobiology of secondary lymphedema remain poorly understood, partly due to the lack of well-described experimental models. Here, we provide a detailed characterization of secondary lymphedema in the mouse tail and correlate the evolution of tissue swelling to changes in tissue architecture, infiltration of immune cells, deposition of lipids, and proliferation and morphology of the lymphatic vessels. We show that sustained swelling leads to lymphatic hyperplasia and upregulation of vascular endothelial growth factor (VEGF)-C, which may exacerbate the edema because the hyperplastic vessels are poorly functional. The onset of lymphatic hyperplasia occurred prior to the onset of lipid accumulation and peak VEGF-C expression. Langerhans dendritic cells were seen in the dermis migrating from the epidermis to the lymphatic capillaries in edematous tissue. Furthermore, these results were consistent between two different normal mouse strains, but swelling was significantly greater in a matrix metalloproteinase (MMP)-9 null strain. Thus, by characterizing this highly reproducible model of secondary lymphedema, we conclude that VEGF-C upregulation and lymphatic hyperplasia resulting from dermal lymphatic ligation and lymphedema leads to decreased drainage function and that MMP-9 may be important in counteracting tissue swelling.</div>
</front>
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<DateCreated><Year>2006</Year>
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<Title>Microvascular research</Title>
<ISOAbbreviation>Microvasc. Res.</ISOAbbreviation>
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<ArticleTitle>Secondary lymphedema in the mouse tail: Lymphatic hyperplasia, VEGF-C upregulation, and the protective role of MMP-9.</ArticleTitle>
<Pagination><MedlinePgn>161-71</MedlinePgn>
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<Abstract><AbstractText>Disturbances in the microcirculation can lead to secondary lymphedema, a common pathological condition that, despite its frequency, still lacks a cure. Lymphedema is clinically well described, but while the genetic underpinnings that cause lymphatic malformations and primary lymphedema are being discovered, the pathophysiology and pathobiology of secondary lymphedema remain poorly understood, partly due to the lack of well-described experimental models. Here, we provide a detailed characterization of secondary lymphedema in the mouse tail and correlate the evolution of tissue swelling to changes in tissue architecture, infiltration of immune cells, deposition of lipids, and proliferation and morphology of the lymphatic vessels. We show that sustained swelling leads to lymphatic hyperplasia and upregulation of vascular endothelial growth factor (VEGF)-C, which may exacerbate the edema because the hyperplastic vessels are poorly functional. The onset of lymphatic hyperplasia occurred prior to the onset of lipid accumulation and peak VEGF-C expression. Langerhans dendritic cells were seen in the dermis migrating from the epidermis to the lymphatic capillaries in edematous tissue. Furthermore, these results were consistent between two different normal mouse strains, but swelling was significantly greater in a matrix metalloproteinase (MMP)-9 null strain. Thus, by characterizing this highly reproducible model of secondary lymphedema, we conclude that VEGF-C upregulation and lymphatic hyperplasia resulting from dermal lymphatic ligation and lymphedema leads to decreased drainage function and that MMP-9 may be important in counteracting tissue swelling.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Rutkowski</LastName>
<ForeName>Joseph M</ForeName>
<Initials>JM</Initials>
<AffiliationInfo><Affiliation>Institute of Bioengineering, Ecole Polytechnique Fédérale de Lausanne (EPFL), Lausanne, Switzerland.</Affiliation>
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<Author ValidYN="Y"><LastName>Moya</LastName>
<ForeName>Monica</ForeName>
<Initials>M</Initials>
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<Author ValidYN="Y"><LastName>Johannes</LastName>
<ForeName>Jimmy</ForeName>
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<Author ValidYN="Y"><LastName>Swartz</LastName>
<ForeName>Melody A</ForeName>
<Initials>MA</Initials>
</Author>
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<Language>eng</Language>
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</MeshHeading>
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</MeshHeading>
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<affiliations><list><country><li>Suisse</li>
</country>
<region><li>Canton de Vaud</li>
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<settlement><li>Lausanne</li>
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<tree><noCountry><name sortKey="Goldman, Jeremy" sort="Goldman, Jeremy" uniqKey="Goldman J" first="Jeremy" last="Goldman">Jeremy Goldman</name>
<name sortKey="Johannes, Jimmy" sort="Johannes, Jimmy" uniqKey="Johannes J" first="Jimmy" last="Johannes">Jimmy Johannes</name>
<name sortKey="Moya, Monica" sort="Moya, Monica" uniqKey="Moya M" first="Monica" last="Moya">Monica Moya</name>
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