Dermal collagen and lipid deposition correlate with tissue swelling and hydraulic conductivity in murine primary lymphedema.
Identifieur interne : 002B81 ( PubMed/Curation ); précédent : 002B80; suivant : 002B82Dermal collagen and lipid deposition correlate with tissue swelling and hydraulic conductivity in murine primary lymphedema.
Auteurs : Joseph M. Rutkowski [Suisse] ; Carl Erik Markhus ; Christina C. Gyenge ; Kari Alitalo ; Helge Wiig ; Melody A. SwartzSource :
- The American journal of pathology [ 1525-2191 ] ; 2010.
Descripteurs français
- KwdFr :
- Animaux, Collagène (métabolisme), Derme (anatomopathologie), Derme (métabolisme), Derme (physiopathologie), Femelle, Humains, Liquide extracellulaire (métabolisme), Lymphoedème (anatomopathologie), Lymphoedème (métabolisme), Lymphoedème (physiopathologie), Modèles animaux de maladie humaine, Mâle, Métabolisme des lipides, Phénomènes biomécaniques, Phénotype, Pression, Récepteur-3 au facteur croissance endothéliale vasculaire (métabolisme), Souris, Souris de lignée C57BL.
- MESH :
- anatomopathologie : Derme, Lymphoedème.
- métabolisme : Collagène, Derme, Liquide extracellulaire, Lymphoedème, Récepteur-3 au facteur croissance endothéliale vasculaire.
- physiopathologie : Derme, Lymphoedème.
- Animaux, Femelle, Humains, Modèles animaux de maladie humaine, Mâle, Métabolisme des lipides, Phénomènes biomécaniques, Phénotype, Pression, Souris, Souris de lignée C57BL.
English descriptors
- KwdEn :
- Animals, Biomechanical Phenomena, Collagen (metabolism), Dermis (metabolism), Dermis (pathology), Dermis (physiopathology), Disease Models, Animal, Extracellular Fluid (metabolism), Female, Humans, Lipid Metabolism, Lymphedema (metabolism), Lymphedema (pathology), Lymphedema (physiopathology), Male, Mice, Mice, Inbred C57BL, Phenotype, Pressure, Vascular Endothelial Growth Factor Receptor-3 (metabolism).
- MESH :
- chemical , metabolism : Collagen, Vascular Endothelial Growth Factor Receptor-3.
- metabolism : Dermis, Extracellular Fluid, Lymphedema.
- pathology : Dermis, Lymphedema.
- physiopathology : Dermis, Lymphedema.
- Animals, Biomechanical Phenomena, Disease Models, Animal, Female, Humans, Lipid Metabolism, Male, Mice, Mice, Inbred C57BL, Phenotype, Pressure.
Abstract
Primary lymphedema is a congenital pathology of dysfunctional lymphatic drainage characterized by swelling of the limbs, thickening of the dermis, and fluid and lipid accumulation in the underlying tissue. Two mouse models of primary lymphedema, the Chy mouse and the K14-VEGFR-3-Ig mouse, both lack dermal lymphatic capillaries and exhibit a lymphedematous phenotype attributable to disrupted VEGFR-3 signaling. Here we show that the differences in edematous tissue composition between these two models correlated with drastic differences in hydraulic conductivity. The skin of Chy mice possessed significantly higher levels of collagen and fat, whereas K14-VEGFR-3-Ig mouse skin composition was relatively normal, as compared with their respective wild-type controls. Functionally, this resulted in a greatly increased dermal hydraulic conductivity in K14-VEGFR3-Ig, but not Chy, mice. Our data suggest that lymphedema associated with increased collagen and lipid accumulation counteracts an increased hydraulic conductivity associated with dermal swelling, which in turn further limits interstitial transport and swelling. Without lipid and collagen accumulation, hydraulic conductivity is increased and overall swelling is minimized. These opposing tissue responses to primary lymphedema imply that tissue remodeling--predominantly collagen and fat deposition--may dictate tissue swelling and govern interstitial transport in lymphedema.
DOI: 10.2353/ajpath.2010.090733
PubMed: 20110415
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Two mouse models of primary lymphedema, the Chy mouse and the K14-VEGFR-3-Ig mouse, both lack dermal lymphatic capillaries and exhibit a lymphedematous phenotype attributable to disrupted VEGFR-3 signaling. Here we show that the differences in edematous tissue composition between these two models correlated with drastic differences in hydraulic conductivity. The skin of Chy mice possessed significantly higher levels of collagen and fat, whereas K14-VEGFR-3-Ig mouse skin composition was relatively normal, as compared with their respective wild-type controls. Functionally, this resulted in a greatly increased dermal hydraulic conductivity in K14-VEGFR3-Ig, but not Chy, mice. Our data suggest that lymphedema associated with increased collagen and lipid accumulation counteracts an increased hydraulic conductivity associated with dermal swelling, which in turn further limits interstitial transport and swelling. Without lipid and collagen accumulation, hydraulic conductivity is increased and overall swelling is minimized. These opposing tissue responses to primary lymphedema imply that tissue remodeling--predominantly collagen and fat deposition--may dictate tissue swelling and govern interstitial transport in lymphedema.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">20110415</PMID><DateCreated><Year>2010</Year><Month>03</Month><Day>10</Day></DateCreated><DateCompleted><Year>2010</Year><Month>06</Month><Day>07</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>22</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1525-2191</ISSN><JournalIssue CitedMedium="Internet"><Volume>176</Volume><Issue>3</Issue><PubDate><Year>2010</Year><Month>Mar</Month></PubDate></JournalIssue><Title>The American journal of pathology</Title><ISOAbbreviation>Am. J. Pathol.</ISOAbbreviation></Journal><ArticleTitle>Dermal collagen and lipid deposition correlate with tissue swelling and hydraulic conductivity in murine primary lymphedema.</ArticleTitle><Pagination><MedlinePgn>1122-9</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.2353/ajpath.2010.090733</ELocationID><Abstract><AbstractText>Primary lymphedema is a congenital pathology of dysfunctional lymphatic drainage characterized by swelling of the limbs, thickening of the dermis, and fluid and lipid accumulation in the underlying tissue. Two mouse models of primary lymphedema, the Chy mouse and the K14-VEGFR-3-Ig mouse, both lack dermal lymphatic capillaries and exhibit a lymphedematous phenotype attributable to disrupted VEGFR-3 signaling. Here we show that the differences in edematous tissue composition between these two models correlated with drastic differences in hydraulic conductivity. The skin of Chy mice possessed significantly higher levels of collagen and fat, whereas K14-VEGFR-3-Ig mouse skin composition was relatively normal, as compared with their respective wild-type controls. Functionally, this resulted in a greatly increased dermal hydraulic conductivity in K14-VEGFR3-Ig, but not Chy, mice. Our data suggest that lymphedema associated with increased collagen and lipid accumulation counteracts an increased hydraulic conductivity associated with dermal swelling, which in turn further limits interstitial transport and swelling. Without lipid and collagen accumulation, hydraulic conductivity is increased and overall swelling is minimized. These opposing tissue responses to primary lymphedema imply that tissue remodeling--predominantly collagen and fat deposition--may dictate tissue swelling and govern interstitial transport in lymphedema.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Rutkowski</LastName><ForeName>Joseph M</ForeName><Initials>JM</Initials><AffiliationInfo><Affiliation>Institute of Bioengineering, School of Life Sciences/LMBM/Station 15, Ecole Polytechnique Fédérale de Lausanne (EPFL), 1015 Lausanne, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Markhus</LastName><ForeName>Carl Erik</ForeName><Initials>CE</Initials></Author><Author ValidYN="Y"><LastName>Gyenge</LastName><ForeName>Christina C</ForeName><Initials>CC</Initials></Author><Author ValidYN="Y"><LastName>Alitalo</LastName><ForeName>Kari</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Wiig</LastName><ForeName>Helge</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Swartz</LastName><ForeName>Melody A</ForeName><Initials>MA</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 HL096539</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL096539-01</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2010</Year><Month>01</Month><Day>28</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Am J Pathol</MedlineTA><NlmUniqueID>0370502</NlmUniqueID><ISSNLinking>0002-9440</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>9007-34-5</RegistryNumber><NameOfSubstance UI="D003094">Collagen</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber><NameOfSubstance UI="D040321">Vascular Endothelial Growth Factor Receptor-3</NameOfSubstance></Chemical></ChemicalList><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Ann Plast Surg. 2007 Oct;59(4):464-72</RefSource><PMID Version="1">17901744</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Dev Dyn. 2007 Aug;236(8):2346-55</RefSource><PMID Version="1">17584866</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Appl Physiol (1985). 2008 Aug;105(2):621-8</RefSource><PMID Version="1">18535138</PMID></CommentsCorrections><CommentsCorrections 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UI="D040321" MajorTopicYN="N">Vascular Endothelial Growth Factor Receptor-3</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">PMC2832135</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2010</Year><Month>1</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2010</Year><Month>1</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2010</Year><Month>6</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">20110415</ArticleId><ArticleId IdType="pii">S0002-9440(10)60426-9</ArticleId><ArticleId IdType="doi">10.2353/ajpath.2010.090733</ArticleId><ArticleId IdType="pmc">PMC2832135</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour 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