Prominent Lymphatic Vessel Hyperplasia with Progressive Dysfunction and Distinct Immune Cell Infiltration in Lymphedema.
Identifieur interne : 000699 ( PubMed/Checkpoint ); précédent : 000698; suivant : 000700Prominent Lymphatic Vessel Hyperplasia with Progressive Dysfunction and Distinct Immune Cell Infiltration in Lymphedema.
Auteurs : Epameinondas Gousopoulos [Suisse] ; Steven T. Proulx [Suisse] ; Jeannette Scholl [Suisse] ; Maja Uecker [Suisse] ; Michael Detmar [Suisse]Source :
- The American journal of pathology [ 1525-2191 ] ; 2016.
Descripteurs français
- KwdFr :
- Animaux, Cellules endothéliales (anatomopathologie), Cellules myéloïdes (anatomopathologie), Cytométrie en flux, Femelle, Hyperplasie (anatomopathologie), Lymphocytes (anatomopathologie), Lymphoedème (anatomopathologie), Modèles animaux de maladie humaine, Queue (anatomopathologie), Souris, Technique d'immunofluorescence, Vaisseaux lymphatiques (anatomopathologie).
- MESH :
English descriptors
- KwdEn :
- MESH :
Abstract
Lymphedema is a common complication that occurs after breast cancer treatment in up to 30% of the patients undergoing surgical lymph node excision. It is associated with tissue swelling, fibrosis, increased risk of infection, and impaired wound healing. Despite the pronounced clinical manifestations of the disease, little is known about the morphological and functional characteristics of the lymphatic vasculature during the course of lymphedema progression. We used an experimental murine tail lymphedema model where sustained fluid stasis was generated on disruption of lymphatic flow, resulting in chronic edema formation with fibrosis and adipose tissue deposition. Morphological analysis of the lymphatic vessels revealed a dramatic expansion during the course of the disease, with active proliferation of lymphatic endothelial cells at the early stages of lymphedema. The lymphatic capillaries exhibited progressively impaired tracer filling and retrograde flow near the surgery site, whereas the collecting lymphatic vessels showed a gradually decreasing contraction amplitude with unchanged contraction frequency, leading to lymphatic contraction arrest at the later stages of the disease. Lymphedema onset was associated with pronounced infiltration by immune cells, predominantly Ly6G(+) and CD4(+) cells, which have been linked to impaired lymphatic vessel function.
DOI: 10.1016/j.ajpath.2016.04.006
PubMed: 27315777
Affiliations:
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Proulx</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, ETH Zurich, Zurich, Switzerland.</nlm:affiliation><country xml:lang="fr">Suisse</country><wicri:regionArea>Institute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, ETH Zurich, Zurich</wicri:regionArea><wicri:noRegion>Zurich</wicri:noRegion></affiliation></author><author><name sortKey="Scholl, Jeannette" sort="Scholl, Jeannette" uniqKey="Scholl J" first="Jeannette" last="Scholl">Jeannette Scholl</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, ETH Zurich, Zurich, Switzerland.</nlm:affiliation><country xml:lang="fr">Suisse</country><wicri:regionArea>Institute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, ETH Zurich, Zurich</wicri:regionArea><wicri:noRegion>Zurich</wicri:noRegion></affiliation></author><author><name sortKey="Uecker, Maja" sort="Uecker, Maja" uniqKey="Uecker M" first="Maja" last="Uecker">Maja Uecker</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, ETH Zurich, Zurich, Switzerland.</nlm:affiliation><country xml:lang="fr">Suisse</country><wicri:regionArea>Institute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, ETH Zurich, Zurich</wicri:regionArea><wicri:noRegion>Zurich</wicri:noRegion></affiliation></author><author><name sortKey="Detmar, Michael" sort="Detmar, Michael" uniqKey="Detmar M" first="Michael" last="Detmar">Michael Detmar</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, ETH Zurich, Zurich, Switzerland. Electronic address: michael.detmar@pharma.ethz.ch.</nlm:affiliation><country xml:lang="fr">Suisse</country><wicri:regionArea>Institute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, ETH Zurich, Zurich</wicri:regionArea><wicri:noRegion>Zurich</wicri:noRegion></affiliation></author></analytic><series><title level="j">The American journal of pathology</title><idno type="eISSN">1525-2191</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Endothelial Cells (pathology)</term><term>Female</term><term>Flow Cytometry</term><term>Fluorescent Antibody Technique</term><term>Hyperplasia (pathology)</term><term>Lymphatic Vessels (pathology)</term><term>Lymphedema (pathology)</term><term>Lymphocytes (pathology)</term><term>Mice</term><term>Myeloid Cells (pathology)</term><term>Tail (pathology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Cellules endothéliales (anatomopathologie)</term><term>Cellules myéloïdes (anatomopathologie)</term><term>Cytométrie en flux</term><term>Femelle</term><term>Hyperplasie (anatomopathologie)</term><term>Lymphocytes (anatomopathologie)</term><term>Lymphoedème (anatomopathologie)</term><term>Modèles animaux de maladie humaine</term><term>Queue (anatomopathologie)</term><term>Souris</term><term>Technique d'immunofluorescence</term><term>Vaisseaux lymphatiques (anatomopathologie)</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Cellules endothéliales</term><term>Cellules myéloïdes</term><term>Hyperplasie</term><term>Lymphocytes</term><term>Lymphoedème</term><term>Queue</term><term>Vaisseaux lymphatiques</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Endothelial Cells</term><term>Hyperplasia</term><term>Lymphatic Vessels</term><term>Lymphedema</term><term>Lymphocytes</term><term>Myeloid Cells</term><term>Tail</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Female</term><term>Flow Cytometry</term><term>Fluorescent Antibody Technique</term><term>Mice</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cytométrie en flux</term><term>Femelle</term><term>Modèles animaux de maladie humaine</term><term>Souris</term><term>Technique d'immunofluorescence</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Lymphedema is a common complication that occurs after breast cancer treatment in up to 30% of the patients undergoing surgical lymph node excision. It is associated with tissue swelling, fibrosis, increased risk of infection, and impaired wound healing. Despite the pronounced clinical manifestations of the disease, little is known about the morphological and functional characteristics of the lymphatic vasculature during the course of lymphedema progression. We used an experimental murine tail lymphedema model where sustained fluid stasis was generated on disruption of lymphatic flow, resulting in chronic edema formation with fibrosis and adipose tissue deposition. Morphological analysis of the lymphatic vessels revealed a dramatic expansion during the course of the disease, with active proliferation of lymphatic endothelial cells at the early stages of lymphedema. The lymphatic capillaries exhibited progressively impaired tracer filling and retrograde flow near the surgery site, whereas the collecting lymphatic vessels showed a gradually decreasing contraction amplitude with unchanged contraction frequency, leading to lymphatic contraction arrest at the later stages of the disease. Lymphedema onset was associated with pronounced infiltration by immune cells, predominantly Ly6G(+) and CD4(+) cells, which have been linked to impaired lymphatic vessel function.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27315777</PMID><DateCreated><Year>2016</Year><Month>07</Month><Day>27</Day></DateCreated><DateCompleted><Year>2017</Year><Month>05</Month><Day>16</Day></DateCompleted><DateRevised><Year>2017</Year><Month>05</Month><Day>16</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1525-2191</ISSN><JournalIssue CitedMedium="Internet"><Volume>186</Volume><Issue>8</Issue><PubDate><Year>2016</Year><Month>Aug</Month></PubDate></JournalIssue><Title>The American journal of pathology</Title><ISOAbbreviation>Am. J. Pathol.</ISOAbbreviation></Journal><ArticleTitle>Prominent Lymphatic Vessel Hyperplasia with Progressive Dysfunction and Distinct Immune Cell Infiltration in Lymphedema.</ArticleTitle><Pagination><MedlinePgn>2193-203</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.ajpath.2016.04.006</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0002-9440(16)30118-3</ELocationID><Abstract><AbstractText>Lymphedema is a common complication that occurs after breast cancer treatment in up to 30% of the patients undergoing surgical lymph node excision. It is associated with tissue swelling, fibrosis, increased risk of infection, and impaired wound healing. Despite the pronounced clinical manifestations of the disease, little is known about the morphological and functional characteristics of the lymphatic vasculature during the course of lymphedema progression. We used an experimental murine tail lymphedema model where sustained fluid stasis was generated on disruption of lymphatic flow, resulting in chronic edema formation with fibrosis and adipose tissue deposition. Morphological analysis of the lymphatic vessels revealed a dramatic expansion during the course of the disease, with active proliferation of lymphatic endothelial cells at the early stages of lymphedema. The lymphatic capillaries exhibited progressively impaired tracer filling and retrograde flow near the surgery site, whereas the collecting lymphatic vessels showed a gradually decreasing contraction amplitude with unchanged contraction frequency, leading to lymphatic contraction arrest at the later stages of the disease. Lymphedema onset was associated with pronounced infiltration by immune cells, predominantly Ly6G(+) and CD4(+) cells, which have been linked to impaired lymphatic vessel function.</AbstractText><CopyrightInformation>Copyright © 2016 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Gousopoulos</LastName><ForeName>Epameinondas</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Institute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, ETH Zurich, Zurich, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Proulx</LastName><ForeName>Steven T</ForeName><Initials>ST</Initials><AffiliationInfo><Affiliation>Institute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, ETH Zurich, Zurich, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Scholl</LastName><ForeName>Jeannette</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Institute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, ETH Zurich, Zurich, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Uecker</LastName><ForeName>Maja</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Institute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, ETH Zurich, Zurich, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Detmar</LastName><ForeName>Michael</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Institute of Pharmaceutical Sciences, Swiss Federal Institute of Technology, ETH Zurich, Zurich, Switzerland. Electronic address: michael.detmar@pharma.ethz.ch.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>06</Month><Day>15</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Am J Pathol</MedlineTA><NlmUniqueID>0370502</NlmUniqueID><ISSNLinking>0002-9440</ISSNLinking></MedlineJournalInfo><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D042783" MajorTopicYN="N">Endothelial Cells</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005434" MajorTopicYN="N">Flow Cytometry</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005455" MajorTopicYN="N">Fluorescent Antibody Technique</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006965" MajorTopicYN="N">Hyperplasia</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D042601" MajorTopicYN="N">Lymphatic Vessels</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008209" MajorTopicYN="N">Lymphedema</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008214" MajorTopicYN="N">Lymphocytes</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D022423" MajorTopicYN="N">Myeloid Cells</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013623" MajorTopicYN="N">Tail</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>12</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2016</Year><Month>02</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>04</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>6</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>6</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>5</Month><Day>17</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27315777</ArticleId><ArticleId IdType="pii">S0002-9440(16)30118-3</ArticleId><ArticleId IdType="doi">10.1016/j.ajpath.2016.04.006</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Suisse</li></country></list><tree><country name="Suisse"><noRegion><name sortKey="Gousopoulos, Epameinondas" sort="Gousopoulos, Epameinondas" uniqKey="Gousopoulos E" first="Epameinondas" last="Gousopoulos">Epameinondas Gousopoulos</name></noRegion><name sortKey="Detmar, Michael" sort="Detmar, Michael" uniqKey="Detmar M" first="Michael" last="Detmar">Michael Detmar</name><name sortKey="Proulx, Steven T" sort="Proulx, Steven T" uniqKey="Proulx S" first="Steven T" last="Proulx">Steven T. Proulx</name><name sortKey="Scholl, Jeannette" sort="Scholl, Jeannette" uniqKey="Scholl J" first="Jeannette" last="Scholl">Jeannette Scholl</name><name sortKey="Uecker, Maja" sort="Uecker, Maja" uniqKey="Uecker M" first="Maja" last="Uecker">Maja Uecker</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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