New Model of Macrophage Acquisition of the Lymphatic Endothelial Phenotype
Identifieur interne : 004096 ( Main/Merge ); précédent : 004095; suivant : 004097New Model of Macrophage Acquisition of the Lymphatic Endothelial Phenotype
Auteurs : Kelly L. Hall ; Lisa D. Volk-Draper ; Michael J. Flister ; Sophia RanSource :
- PLoS ONE [ 1932-6203 ] ; 2012.
Abstract
Macrophage-derived lymphatic endothelial cell progenitors (M-LECPs) contribute to new lymphatic vessel formation, but the mechanisms regulating their differentiation, recruitment, and function are poorly understood. Detailed characterization of M-LECPs is limited by low frequency
Time-course analysis of diaphragms from lipopolysaccharide (LPS)-treated mice revealed rapid mobilization of bone marrow-derived and peritoneal macrophages to the proximity of lymphatic vessels followed by widespread (∼50%) incorporation of M-LECPs into the inflamed lymphatic vasculature. A differentiation shift toward the lymphatic phenotype was found in three LPS-induced subsets of activated macrophages that were positive for VEGFR-3 and many other lymphatic-specific markers. VEGFR-3 was strongly elevated in the early stage of macrophage transition to LECPs but undetectable in M-LECPs prior to vascular integration. Similar transient pattern of VEGFR-3 expression was found in RAW264.7 macrophages activated by LPS
We present a new model for macrophage-LECP differentiation based on LPS activation of cultured RAW264.7 cells. This system designated here as the “RAW model” mimics fundamental features of endogenous M-LECPs. Unlike native LECPs, this model is unrestricted by cell numbers, heterogeneity of population, and ability to change genetic composition for experimental purposes. As such, this model can provide a valuable tool for understanding the LECP and lymphatic biology.
Url:
DOI: 10.1371/journal.pone.0031794
PubMed: 22396739
PubMed Central: 3292559
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">New Model of Macrophage Acquisition of the Lymphatic Endothelial Phenotype</title><author><name sortKey="Hall, Kelly L" sort="Hall, Kelly L" uniqKey="Hall K" first="Kelly L." last="Hall">Kelly L. Hall</name></author><author><name sortKey="Volk Draper, Lisa D" sort="Volk Draper, Lisa D" uniqKey="Volk Draper L" first="Lisa D." last="Volk-Draper">Lisa D. Volk-Draper</name></author><author><name sortKey="Flister, Michael J" sort="Flister, Michael J" uniqKey="Flister M" first="Michael J." last="Flister">Michael J. Flister</name></author><author><name sortKey="Ran, Sophia" sort="Ran, Sophia" uniqKey="Ran S" first="Sophia" last="Ran">Sophia Ran</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">22396739</idno><idno type="pmc">3292559</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3292559</idno><idno type="RBID">PMC:3292559</idno><idno type="doi">10.1371/journal.pone.0031794</idno><date when="2012">2012</date><idno type="wicri:Area/Pmc/Corpus">004529</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">004529</idno><idno type="wicri:Area/Pmc/Curation">004528</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">004528</idno><idno type="wicri:Area/Pmc/Checkpoint">002859</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">002859</idno><idno type="wicri:Area/Ncbi/Merge">004B57</idno><idno type="wicri:Area/Ncbi/Curation">004B57</idno><idno type="wicri:Area/Ncbi/Checkpoint">004B57</idno><idno type="wicri:Area/Main/Merge">004096</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">New Model of Macrophage Acquisition of the Lymphatic Endothelial Phenotype</title><author><name sortKey="Hall, Kelly L" sort="Hall, Kelly L" uniqKey="Hall K" first="Kelly L." last="Hall">Kelly L. Hall</name></author><author><name sortKey="Volk Draper, Lisa D" sort="Volk Draper, Lisa D" uniqKey="Volk Draper L" first="Lisa D." last="Volk-Draper">Lisa D. Volk-Draper</name></author><author><name sortKey="Flister, Michael J" sort="Flister, Michael J" uniqKey="Flister M" first="Michael J." last="Flister">Michael J. Flister</name></author><author><name sortKey="Ran, Sophia" sort="Ran, Sophia" uniqKey="Ran S" first="Sophia" last="Ran">Sophia Ran</name><affiliation><nlm:aff id="aff1"></nlm:aff></affiliation></author></analytic><series><title level="j">PLoS ONE</title><idno type="eISSN">1932-6203</idno><imprint><date when="2012">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec><title>Background</title><p>Macrophage-derived lymphatic endothelial cell progenitors (M-LECPs) contribute to new lymphatic vessel formation, but the mechanisms regulating their differentiation, recruitment, and function are poorly understood. Detailed characterization of M-LECPs is limited by low frequency <italic>in vivo</italic> and lack of model systems allowing in-depth molecular analyses <italic>in vitro</italic>. Our goal was to establish a cell culture model to characterize inflammation-induced macrophage-to-LECP differentiation under controlled conditions.</p></sec><sec><title>Methodology/Principal Findings</title><p>Time-course analysis of diaphragms from lipopolysaccharide (LPS)-treated mice revealed rapid mobilization of bone marrow-derived and peritoneal macrophages to the proximity of lymphatic vessels followed by widespread (∼50%) incorporation of M-LECPs into the inflamed lymphatic vasculature. A differentiation shift toward the lymphatic phenotype was found in three LPS-induced subsets of activated macrophages that were positive for VEGFR-3 and many other lymphatic-specific markers. VEGFR-3 was strongly elevated in the early stage of macrophage transition to LECPs but undetectable in M-LECPs prior to vascular integration. Similar transient pattern of VEGFR-3 expression was found in RAW264.7 macrophages activated by LPS <italic>in vitro</italic>. Activated RAW264.7 cells co-expressed VEGF-C that induced an autocrine signaling loop as indicated by VEGFR-3 phosphorylation inhibited by a soluble receptor. LPS-activated RAW264.7 macrophages also showed a 68% overlap with endogenous CD11b<sup>+</sup>/VEGFR-3<sup>+</sup> LECPs in the expression of lymphatic-specific genes. Moreover, when injected into LPS- but not saline-treated mice, GFP-tagged RAW264.7 cells massively infiltrated the inflamed diaphragm followed by integration into 18% of lymphatic vessels.</p></sec><sec><title>Conclusions/Significance</title><p>We present a new model for macrophage-LECP differentiation based on LPS activation of cultured RAW264.7 cells. This system designated here as the “RAW model” mimics fundamental features of endogenous M-LECPs. Unlike native LECPs, this model is unrestricted by cell numbers, heterogeneity of population, and ability to change genetic composition for experimental purposes. 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M">M Natarajan</name></author><author><name sortKey="Lin, Km" uniqKey="Lin K">KM Lin</name></author><author><name sortKey="Hsueh, Rc" uniqKey="Hsueh R">RC Hsueh</name></author><author><name sortKey="Sternweis, Pc" uniqKey="Sternweis P">PC Sternweis</name></author><author><name sortKey="Ranganathan, R" uniqKey="Ranganathan R">R Ranganathan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Schmittgen, Td" uniqKey="Schmittgen T">TD Schmittgen</name></author><author><name sortKey="Livak, Kj" uniqKey="Livak K">KJ Livak</name></author></analytic></biblStruct></listBibl></div1></back></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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