Regulation of Adipogenesis by Lymphatic fluid Stasis Part II: Expression of Adipose Differentiation Genes
Identifieur interne : 003F24 ( Main/Exploration ); précédent : 003F23; suivant : 003F25Regulation of Adipogenesis by Lymphatic fluid Stasis Part II: Expression of Adipose Differentiation Genes
Auteurs : Seth Aschen [États-Unis] ; Jamie C. Zampell [États-Unis] ; Sonia Elhadad [États-Unis] ; Evan Weitman [États-Unis] ; Marina De Brot Andrade [États-Unis] ; Babak J. Mehrara [États-Unis]Source :
- Plastic and reconstructive surgery [ 0032-1052 ] ; 2012.
Descripteurs français
- KwdFr :
- Adipocytes (cytologie), Adipogenèse (génétique), Adiponectine (génétique), Adiponectine (métabolisme), Aisselle, Animaux, Différenciation cellulaire (génétique), Femelle, Fibrose, Graisse sous-cutanée (physiologie), Immunohistochimie, Lymphadénectomie (effets indésirables), Lymphe (physiologie), Lymphoedème (génétique), Lymphoedème (physiopathologie), Lymphoedème (étiologie), Membre thoracique, Modèles animaux de maladie humaine, Protéine bêta de liaison aux séquences stimulatrices de type CCAAT (génétique), Protéine bêta de liaison aux séquences stimulatrices de type CCAAT (métabolisme), Queue, Récepteur PPAR gamma (génétique), Récepteur PPAR gamma (métabolisme), Régulation de l'expression des gènes, Régulation positive, Souris, Souris de lignée C57BL.
- MESH :
- cytologie : Adipocytes.
- effets indésirables : Lymphadénectomie.
- génétique : Adipogenèse, Adiponectine, Différenciation cellulaire, Lymphoedème, Protéine bêta de liaison aux séquences stimulatrices de type CCAAT, Récepteur PPAR gamma.
- métabolisme : Adiponectine, Protéine bêta de liaison aux séquences stimulatrices de type CCAAT, Récepteur PPAR gamma.
- physiologie : Graisse sous-cutanée, Lymphe.
- physiopathologie : Lymphoedème.
- étiologie : Lymphoedème.
- Aisselle, Animaux, Femelle, Fibrose, Immunohistochimie, Membre thoracique, Modèles animaux de maladie humaine, Queue, Régulation de l'expression des gènes, Régulation positive, Souris, Souris de lignée C57BL.
English descriptors
- KwdEn :
- Adipocytes (cytology), Adipogenesis (genetics), Adiponectin (genetics), Adiponectin (metabolism), Animals, Axilla, CCAAT-Enhancer-Binding Protein-beta (genetics), CCAAT-Enhancer-Binding Protein-beta (metabolism), Cell Differentiation (genetics), Disease Models, Animal, Female, Fibrosis, Forelimb, Gene Expression Regulation, Immunohistochemistry, Lymph (physiology), Lymph Node Excision (adverse effects), Lymphedema (etiology), Lymphedema (genetics), Lymphedema (physiopathology), Mice, Mice, Inbred C57BL, PPAR gamma (genetics), PPAR gamma (metabolism), Subcutaneous Fat (physiology), Tail, Up-Regulation.
- MESH :
- chemical , genetics : Adiponectin, CCAAT-Enhancer-Binding Protein-beta, PPAR gamma.
- adverse effects : Lymph Node Excision.
- cytology : Adipocytes.
- etiology : Lymphedema.
- genetics : Adipogenesis, Cell Differentiation, Lymphedema.
- chemical , metabolism : Adiponectin, CCAAT-Enhancer-Binding Protein-beta, PPAR gamma.
- physiology : Lymph, Subcutaneous Fat.
- physiopathology : Lymphedema.
- Animals, Axilla, Disease Models, Animal, Female, Fibrosis, Forelimb, Gene Expression Regulation, Immunohistochemistry, Mice, Mice, Inbred C57BL, Tail, Up-Regulation.
Abstract
Although fat deposition is a defining clinical characteristic of lymphedema, the cellular mechanisms that regulate this response remain unknown. The goal of this study was to determine how lymphatic fluid stasis regulates adipogenic gene activation and fat deposition.
Adult female mice underwent tail lymphatic ablation and sacrifice at 1, 3, or 6 weeks post-operatively (n=8/group). Samples were analyzed by immunohistochemistry and western blot. An alternative group of mice underwent axillary dissections or sham incisions and limb tissues were harvested 3 weeks post-operatively (n=8/group).
Lymphatic fluid stasis resulted in significant subcutaneous fat deposition and fibrosis in lymphedematous tail regions (p<0.001). Western blot analysis demonstrated that proteins regulating adipose differentiation including CCAAT/enhancer binding protein-alpha (CEBP-α) and adiponectin were markedly upregulated in response to lymphatic fluid stasis in the tail and axillary models. Expression of these markers increased in edematous tissues according to the gradient of lymphatic stasis distal to the wound. Immunohistochemical analysis further demonstrated that adiponectin and peroxisome proliferator-activated receptor gamma (PPAR-γ), another critical adipogenic transcription factor, followed similar expression gradients. Finally, adiponectin and PPAR-γ expression localized to a variety of cell types in newly formed subcutaneous fat.
The mouse-tail model of lymphedema demonstrates pathological findings similar to clinical lymphedema including fat deposition and fibrosis. We show that lymphatic fluid stasis potently upregulates the expression of fat differentiation markers both spatially and temporally. These studies elucidate mechanisms regulating abnormal fat deposition in lymphedema pathogenesis and therefore provide a basis for developing targeted treatments.
Url:
DOI: 10.1097/PRS.0b013e3182450b47
PubMed: 22456356
PubMed Central: 3445411
Affiliations:
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Mehrara</name><affiliation wicri:level="2"><nlm:aff id="A1">The Division of Plastic and Reconstructive Surgery, Memorial Sloan-Kettering Cancer Center, New York, NY 10065</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">État de New York</region></placeName><wicri:cityArea>The Division of Plastic and Reconstructive Surgery, Memorial Sloan-Kettering Cancer Center, New York</wicri:cityArea></affiliation></author></analytic><series><title level="j">Plastic and reconstructive surgery</title><idno type="ISSN">0032-1052</idno><idno type="eISSN">1529-4242</idno><imprint><date when="2012">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adipocytes (cytology)</term><term>Adipogenesis (genetics)</term><term>Adiponectin (genetics)</term><term>Adiponectin (metabolism)</term><term>Animals</term><term>Axilla</term><term>CCAAT-Enhancer-Binding Protein-beta (genetics)</term><term>CCAAT-Enhancer-Binding Protein-beta (metabolism)</term><term>Cell Differentiation (genetics)</term><term>Disease Models, Animal</term><term>Female</term><term>Fibrosis</term><term>Forelimb</term><term>Gene Expression Regulation</term><term>Immunohistochemistry</term><term>Lymph (physiology)</term><term>Lymph Node Excision (adverse effects)</term><term>Lymphedema (etiology)</term><term>Lymphedema (genetics)</term><term>Lymphedema (physiopathology)</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>PPAR gamma (genetics)</term><term>PPAR gamma (metabolism)</term><term>Subcutaneous Fat (physiology)</term><term>Tail</term><term>Up-Regulation</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adipocytes (cytologie)</term><term>Adipogenèse (génétique)</term><term>Adiponectine (génétique)</term><term>Adiponectine (métabolisme)</term><term>Aisselle</term><term>Animaux</term><term>Différenciation cellulaire (génétique)</term><term>Femelle</term><term>Fibrose</term><term>Graisse sous-cutanée (physiologie)</term><term>Immunohistochimie</term><term>Lymphadénectomie (effets indésirables)</term><term>Lymphe (physiologie)</term><term>Lymphoedème (génétique)</term><term>Lymphoedème (physiopathologie)</term><term>Lymphoedème (étiologie)</term><term>Membre thoracique</term><term>Modèles animaux de maladie humaine</term><term>Protéine bêta de liaison aux séquences stimulatrices de type CCAAT (génétique)</term><term>Protéine bêta de liaison aux séquences stimulatrices de type CCAAT (métabolisme)</term><term>Queue</term><term>Récepteur PPAR gamma (génétique)</term><term>Récepteur PPAR gamma (métabolisme)</term><term>Régulation de l'expression des gènes</term><term>Régulation positive</term><term>Souris</term><term>Souris de lignée C57BL</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Adiponectin</term><term>CCAAT-Enhancer-Binding Protein-beta</term><term>PPAR gamma</term></keywords><keywords scheme="MESH" qualifier="adverse effects" xml:lang="en"><term>Lymph Node Excision</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Adipocytes</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Adipocytes</term></keywords><keywords scheme="MESH" qualifier="effets indésirables" xml:lang="fr"><term>Lymphadénectomie</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Lymphedema</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Adipogenesis</term><term>Cell Differentiation</term><term>Lymphedema</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Adipogenèse</term><term>Adiponectine</term><term>Différenciation cellulaire</term><term>Lymphoedème</term><term>Protéine bêta de liaison aux séquences stimulatrices de type CCAAT</term><term>Récepteur PPAR gamma</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Adiponectin</term><term>CCAAT-Enhancer-Binding Protein-beta</term><term>PPAR gamma</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Adiponectine</term><term>Protéine bêta de liaison aux séquences stimulatrices de type CCAAT</term><term>Récepteur PPAR gamma</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Graisse sous-cutanée</term><term>Lymphe</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Lymph</term><term>Subcutaneous Fat</term></keywords><keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Lymphoedème</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Lymphedema</term></keywords><keywords scheme="MESH" qualifier="étiologie" xml:lang="fr"><term>Lymphoedème</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Axilla</term><term>Disease Models, Animal</term><term>Female</term><term>Fibrosis</term><term>Forelimb</term><term>Gene Expression Regulation</term><term>Immunohistochemistry</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Tail</term><term>Up-Regulation</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Aisselle</term><term>Animaux</term><term>Femelle</term><term>Fibrose</term><term>Immunohistochimie</term><term>Membre thoracique</term><term>Modèles animaux de maladie humaine</term><term>Queue</term><term>Régulation de l'expression des gènes</term><term>Régulation positive</term><term>Souris</term><term>Souris de lignée C57BL</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec id="S1"><title>Background</title><p id="P1">Although fat deposition is a defining clinical characteristic of lymphedema, the cellular mechanisms that regulate this response remain unknown. The goal of this study was to determine how lymphatic fluid stasis regulates adipogenic gene activation and fat deposition.</p></sec><sec id="S2"><title>Methods</title><p id="P2">Adult female mice underwent tail lymphatic ablation and sacrifice at 1, 3, or 6 weeks post-operatively (n=8/group). Samples were analyzed by immunohistochemistry and western blot. An alternative group of mice underwent axillary dissections or sham incisions and limb tissues were harvested 3 weeks post-operatively (n=8/group).</p></sec><sec id="S3"><title>Results</title><p id="P3">Lymphatic fluid stasis resulted in significant subcutaneous fat deposition and fibrosis in lymphedematous tail regions (p<0.001). Western blot analysis demonstrated that proteins regulating adipose differentiation including CCAAT/enhancer binding protein-alpha (CEBP-α) and adiponectin were markedly upregulated in response to lymphatic fluid stasis in the tail and axillary models. Expression of these markers increased in edematous tissues according to the gradient of lymphatic stasis distal to the wound. Immunohistochemical analysis further demonstrated that adiponectin and peroxisome proliferator-activated receptor gamma (PPAR-γ), another critical adipogenic transcription factor, followed similar expression gradients. Finally, adiponectin and PPAR-γ expression localized to a variety of cell types in newly formed subcutaneous fat.</p></sec><sec id="S4"><title>Conclusions</title><p id="P4">The mouse-tail model of lymphedema demonstrates pathological findings similar to clinical lymphedema including fat deposition and fibrosis. We show that lymphatic fluid stasis potently upregulates the expression of fat differentiation markers both spatially and temporally. These studies elucidate mechanisms regulating abnormal fat deposition in lymphedema pathogenesis and therefore provide a basis for developing targeted treatments.</p></sec></div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>État de New York</li></region></list><tree><country name="États-Unis"><region name="État de New York"><name sortKey="Aschen, Seth" sort="Aschen, Seth" uniqKey="Aschen S" first="Seth" last="Aschen">Seth Aschen</name></region><name sortKey="De Brot Andrade, Marina" sort="De Brot Andrade, Marina" uniqKey="De Brot Andrade M" first="Marina" last="De Brot Andrade">Marina De Brot Andrade</name><name sortKey="Elhadad, Sonia" sort="Elhadad, Sonia" uniqKey="Elhadad S" first="Sonia" last="Elhadad">Sonia Elhadad</name><name sortKey="Mehrara, Babak J" sort="Mehrara, Babak J" uniqKey="Mehrara B" first="Babak J." last="Mehrara">Babak J. Mehrara</name><name sortKey="Weitman, Evan" sort="Weitman, Evan" uniqKey="Weitman E" first="Evan" last="Weitman">Evan Weitman</name><name sortKey="Zampell, Jamie C" sort="Zampell, Jamie C" uniqKey="Zampell J" first="Jamie C." last="Zampell">Jamie C. Zampell</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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