Blockade of transforming growth factor-beta1 accelerates lymphatic regeneration during wound repair.
Identifieur interne : 002943 ( PubMed/Checkpoint ); précédent : 002942; suivant : 002944Blockade of transforming growth factor-beta1 accelerates lymphatic regeneration during wound repair.
Auteurs : Tomer Avraham [États-Unis] ; Sanjay Daluvoy ; Jaime Zampell ; Alan Yan ; Yosef S. Haviv ; Stanley G. Rockson ; Babak J. MehraraSource :
- The American journal of pathology [ 1525-2191 ] ; 2010.
Descripteurs français
- KwdFr :
- Animaux, Anticorps monoclonaux (pharmacologie), Cellules cultivées, Cicatrisation de plaie (), Cicatrisation de plaie (immunologie), Cicatrisation de plaie (physiologie), Facteur de croissance transformant bêta-1 (antagonistes et inhibiteurs), Facteur de croissance transformant bêta-1 (immunologie), Facteur de croissance transformant bêta-1 (métabolisme), Femelle, Fibrose (anatomopathologie), Humains, Lymphangiogenèse (), Lymphangiogenèse (immunologie), Lymphangiogenèse (physiologie), Lymphocytes auxiliaires Th2 (), Lymphocytes auxiliaires Th2 (physiologie), Lymphoedème (anatomopathologie), Lymphoedème (immunologie), Lymphoedème (métabolisme), Régulation positive (), Régulation positive (immunologie), Régulation positive (physiologie), Régénération (), Régénération (immunologie), Régénération (physiologie), Souris, Souris de lignée C57BL, Vaisseaux lymphatiques (), Vaisseaux lymphatiques (immunologie), Vaisseaux lymphatiques (métabolisme), Vaisseaux lymphatiques (physiopathologie).
- MESH :
- anatomopathologie : Fibrose, Lymphoedème.
- antagonistes et inhibiteurs : Facteur de croissance transformant bêta-1.
- immunologie : Cicatrisation de plaie, Facteur de croissance transformant bêta-1, Lymphangiogenèse, Lymphoedème, Régulation positive, Régénération, Vaisseaux lymphatiques.
- métabolisme : Facteur de croissance transformant bêta-1, Lymphoedème, Vaisseaux lymphatiques.
- pharmacologie : Anticorps monoclonaux.
- physiologie : Cicatrisation de plaie, Lymphangiogenèse, Lymphocytes auxiliaires Th2, Régulation positive, Régénération.
- physiopathologie : Vaisseaux lymphatiques.
- Animaux, Cellules cultivées, Cicatrisation de plaie, Femelle, Humains, Lymphangiogenèse, Lymphocytes auxiliaires Th2, Régulation positive, Régénération, Souris, Souris de lignée C57BL, Vaisseaux lymphatiques.
English descriptors
- KwdEn :
- Animals, Antibodies, Monoclonal (pharmacology), Cells, Cultured, Female, Fibrosis (pathology), Humans, Lymphangiogenesis (drug effects), Lymphangiogenesis (immunology), Lymphangiogenesis (physiology), Lymphatic Vessels (drug effects), Lymphatic Vessels (immunology), Lymphatic Vessels (metabolism), Lymphatic Vessels (physiopathology), Lymphedema (immunology), Lymphedema (metabolism), Lymphedema (pathology), Mice, Mice, Inbred C57BL, Regeneration (drug effects), Regeneration (immunology), Regeneration (physiology), Th2 Cells (drug effects), Th2 Cells (physiology), Transforming Growth Factor beta1 (antagonists & inhibitors), Transforming Growth Factor beta1 (immunology), Transforming Growth Factor beta1 (metabolism), Up-Regulation (drug effects), Up-Regulation (immunology), Up-Regulation (physiology), Wound Healing (drug effects), Wound Healing (immunology), Wound Healing (physiology).
- MESH :
- chemical , antagonists & inhibitors : Transforming Growth Factor beta1.
- chemical , immunology : Transforming Growth Factor beta1.
- chemical , metabolism : Transforming Growth Factor beta1.
- chemical , pharmacology : Antibodies, Monoclonal.
- drug effects : Lymphangiogenesis, Lymphatic Vessels, Regeneration, Th2 Cells, Up-Regulation, Wound Healing.
- immunology : Lymphangiogenesis, Lymphatic Vessels, Lymphedema, Regeneration, Up-Regulation, Wound Healing.
- metabolism : Lymphatic Vessels, Lymphedema.
- pathology : Fibrosis, Lymphedema.
- physiology : Lymphangiogenesis, Regeneration, Th2 Cells, Up-Regulation, Wound Healing.
- physiopathology : Lymphatic Vessels.
- Animals, Cells, Cultured, Female, Humans, Mice, Mice, Inbred C57BL.
Abstract
Lymphedema is a complication of cancer treatment occurring in approximately 50% of patients who undergo lymph node resection. Despite its prevalence, the etiology of this disorder remains unknown. In this study, we determined the effect of soft tissue fibrosis on lymphatic function and the role of transforming growth factor (TGF)-β1 in the regulation of this response. We determined TGF-β expression patterns in matched biopsy specimens collected from lymphedematous and normal limbs of patients with secondary lymphedema. To determine the role of TGF-β in regulating tissue fibrosis, we used a mouse model of lymphedema and inhibited TGF-β function either systemically with a monoclonal antibody or locally by using a soluble, defective TGF-β receptor. Lymphedematous tissue demonstrated a nearly threefold increase in the number of cells that stained for TGF-β1. TGF-β inhibition markedly decreased tissue fibrosis, increased lymphangiogenesis, and improved lymphatic function compared with controls. In addition, inhibition of TGF-β not only decreased TGF-β expression in lymphedematous tissues, but also diminished inflammation, migration of T-helper type 2 (Th2) cells, and expression of profibrotic Th2 cytokines. Similarly, systemic depletion of T-cells markedly decreased TGF-β expression in tail tissues. Inhibition of TGF-β function promoted lymphatic regeneration, decreased tissue fibrosis, decreased chronic inflammation and Th2 cell migration, and improved lymphatic function. The use of these strategies may represent a novel means of preventing lymphedema after lymph node resection.
DOI: 10.2353/ajpath.2010.100594
PubMed: 21056998
Affiliations:
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C57BL</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules cultivées</term><term>Cicatrisation de plaie</term><term>Femelle</term><term>Humains</term><term>Lymphangiogenèse</term><term>Lymphocytes auxiliaires Th2</term><term>Régulation positive</term><term>Régénération</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Vaisseaux lymphatiques</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Lymphedema is a complication of cancer treatment occurring in approximately 50% of patients who undergo lymph node resection. Despite its prevalence, the etiology of this disorder remains unknown. In this study, we determined the effect of soft tissue fibrosis on lymphatic function and the role of transforming growth factor (TGF)-β1 in the regulation of this response. We determined TGF-β expression patterns in matched biopsy specimens collected from lymphedematous and normal limbs of patients with secondary lymphedema. To determine the role of TGF-β in regulating tissue fibrosis, we used a mouse model of lymphedema and inhibited TGF-β function either systemically with a monoclonal antibody or locally by using a soluble, defective TGF-β receptor. Lymphedematous tissue demonstrated a nearly threefold increase in the number of cells that stained for TGF-β1. TGF-β inhibition markedly decreased tissue fibrosis, increased lymphangiogenesis, and improved lymphatic function compared with controls. In addition, inhibition of TGF-β not only decreased TGF-β expression in lymphedematous tissues, but also diminished inflammation, migration of T-helper type 2 (Th2) cells, and expression of profibrotic Th2 cytokines. Similarly, systemic depletion of T-cells markedly decreased TGF-β expression in tail tissues. Inhibition of TGF-β function promoted lymphatic regeneration, decreased tissue fibrosis, decreased chronic inflammation and Th2 cell migration, and improved lymphatic function. The use of these strategies may represent a novel means of preventing lymphedema after lymph node resection.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">21056998</PMID><DateCreated><Year>2010</Year><Month>12</Month><Day>01</Day></DateCreated><DateCompleted><Year>2011</Year><Month>03</Month><Day>15</Day></DateCompleted><DateRevised><Year>2016</Year><Month>10</Month><Day>19</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1525-2191</ISSN><JournalIssue CitedMedium="Internet"><Volume>177</Volume><Issue>6</Issue><PubDate><Year>2010</Year><Month>Dec</Month></PubDate></JournalIssue><Title>The American journal of pathology</Title><ISOAbbreviation>Am. J. Pathol.</ISOAbbreviation></Journal><ArticleTitle>Blockade of transforming growth factor-beta1 accelerates lymphatic regeneration during wound repair.</ArticleTitle><Pagination><MedlinePgn>3202-14</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.2353/ajpath.2010.100594</ELocationID><Abstract><AbstractText>Lymphedema is a complication of cancer treatment occurring in approximately 50% of patients who undergo lymph node resection. Despite its prevalence, the etiology of this disorder remains unknown. In this study, we determined the effect of soft tissue fibrosis on lymphatic function and the role of transforming growth factor (TGF)-β1 in the regulation of this response. We determined TGF-β expression patterns in matched biopsy specimens collected from lymphedematous and normal limbs of patients with secondary lymphedema. To determine the role of TGF-β in regulating tissue fibrosis, we used a mouse model of lymphedema and inhibited TGF-β function either systemically with a monoclonal antibody or locally by using a soluble, defective TGF-β receptor. Lymphedematous tissue demonstrated a nearly threefold increase in the number of cells that stained for TGF-β1. TGF-β inhibition markedly decreased tissue fibrosis, increased lymphangiogenesis, and improved lymphatic function compared with controls. In addition, inhibition of TGF-β not only decreased TGF-β expression in lymphedematous tissues, but also diminished inflammation, migration of T-helper type 2 (Th2) cells, and expression of profibrotic Th2 cytokines. Similarly, systemic depletion of T-cells markedly decreased TGF-β expression in tail tissues. Inhibition of TGF-β function promoted lymphatic regeneration, decreased tissue fibrosis, decreased chronic inflammation and Th2 cell migration, and improved lymphatic function. The use of these strategies may represent a novel means of preventing lymphedema after lymph node resection.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Avraham</LastName><ForeName>Tomer</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>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>Daluvoy</LastName><ForeName>Sanjay</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Zampell</LastName><ForeName>Jaime</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Yan</LastName><ForeName>Alan</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Haviv</LastName><ForeName>Yosef S</ForeName><Initials>YS</Initials></Author><Author ValidYN="Y"><LastName>Rockson</LastName><ForeName>Stanley G</ForeName><Initials>SG</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>P30 CA08748</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P30 CA008748</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R24 CA83084</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 CA 009501</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R24 CA083084</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>2010</Year><Month>11</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Am J Pathol</MedlineTA><NlmUniqueID>0370502</NlmUniqueID><ISSNLinking>0002-9440</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000911">Antibodies, Monoclonal</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D053773">Transforming Growth Factor beta1</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Lab Invest. 2007 Nov;87(11):1077-91</RefSource><PMID 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MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D042583" MajorTopicYN="N">Lymphangiogenesis</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D042601" MajorTopicYN="N">Lymphatic Vessels</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008209" MajorTopicYN="N">Lymphedema</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012038" MajorTopicYN="N">Regeneration</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018418" MajorTopicYN="N">Th2 Cells</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D053773" MajorTopicYN="N">Transforming Growth Factor beta1</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="Y">antagonists & inhibitors</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015854" MajorTopicYN="N">Up-Regulation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014945" MajorTopicYN="N">Wound Healing</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">PMC2993295</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2010</Year><Month>11</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2010</Year><Month>11</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2011</Year><Month>3</Month><Day>16</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">21056998</ArticleId><ArticleId IdType="pii">S0002-9440(10)62943-4</ArticleId><ArticleId IdType="doi">10.2353/ajpath.2010.100594</ArticleId><ArticleId IdType="pmc">PMC2993295</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>État de New York</li></region></list><tree><noCountry><name sortKey="Daluvoy, Sanjay" sort="Daluvoy, Sanjay" uniqKey="Daluvoy S" first="Sanjay" last="Daluvoy">Sanjay Daluvoy</name><name sortKey="Haviv, Yosef S" sort="Haviv, Yosef S" uniqKey="Haviv Y" first="Yosef S" last="Haviv">Yosef S. Haviv</name><name sortKey="Mehrara, Babak J" sort="Mehrara, Babak J" uniqKey="Mehrara B" first="Babak J" last="Mehrara">Babak J. Mehrara</name><name sortKey="Rockson, Stanley G" sort="Rockson, Stanley G" uniqKey="Rockson S" first="Stanley G" last="Rockson">Stanley G. Rockson</name><name sortKey="Yan, Alan" sort="Yan, Alan" uniqKey="Yan A" first="Alan" last="Yan">Alan Yan</name><name sortKey="Zampell, Jaime" sort="Zampell, Jaime" uniqKey="Zampell J" first="Jaime" last="Zampell">Jaime Zampell</name></noCountry><country name="États-Unis"><region name="État de New York"><name sortKey="Avraham, Tomer" sort="Avraham, Tomer" uniqKey="Avraham T" first="Tomer" last="Avraham">Tomer Avraham</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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