Lymphatic vasculature mediates macrophage reverse cholesterol transport in mice
Identifieur interne : 002F20 ( Pmc/Curation ); précédent : 002F19; suivant : 002F21Lymphatic vasculature mediates macrophage reverse cholesterol transport in mice
Auteurs : Catherine Martel [États-Unis] ; Wenjun Li [États-Unis] ; Brian Fulp [États-Unis] ; Andrew M. Platt [États-Unis] ; Emmanuel L. Gautier ; Marit Westerterp [États-Unis] ; Robert Bittman [États-Unis] ; Alan R. Tall [États-Unis] ; Shu-Hsia Chen [États-Unis] ; Michael J. Thomas [États-Unis] ; Daniel Kreisel [États-Unis] ; Melody A. Swartz [Suisse] ; Mary G. Sorci-Thomas [États-Unis] ; Gwendalyn J. Randolph [États-Unis]Source :
- The Journal of Clinical Investigation [ 0021-9738 ] ; 2013.
Abstract
Reverse cholesterol transport (RCT) refers to the mobilization of cholesterol on HDL particles (HDL-C) from extravascular tissues to plasma, ultimately for fecal excretion. Little is known about how HDL-C leaves peripheral tissues to reach plasma. We first used 2 models of disrupted lymphatic drainage from skin — 1 surgical and the other genetic — to quantitatively track RCT following injection of [3H]-cholesterol–loaded macrophages upstream of blocked or absent lymphatic vessels. Macrophage RCT was markedly impaired in both models, even at sites with a leaky vasculature. Inhibited RCT was downstream of cholesterol efflux from macrophages, since macrophage efflux of a fluorescent cholesterol analog (BODIPY-cholesterol) was not altered by impaired lymphatic drainage. We next addressed whether RCT was mediated by lymphatic vessels from the aortic wall by loading the aortae of donor atherosclerotic
Url:
DOI: 10.1172/JCI63685
PubMed: 23524964
PubMed Central: 3613904
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<author><name sortKey="Randolph, Gwendalyn J" sort="Randolph, Gwendalyn J" uniqKey="Randolph G" first="Gwendalyn J." last="Randolph">Gwendalyn J. Randolph</name>
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<idno type="ISSN">0021-9738</idno>
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<front><div type="abstract" xml:lang="en"><p>Reverse cholesterol transport (RCT) refers to the mobilization of cholesterol on HDL particles (HDL-C) from extravascular tissues to plasma, ultimately for fecal excretion. Little is known about how HDL-C leaves peripheral tissues to reach plasma. We first used 2 models of disrupted lymphatic drainage from skin — 1 surgical and the other genetic — to quantitatively track RCT following injection of [<sup>3</sup>
H]-cholesterol–loaded macrophages upstream of blocked or absent lymphatic vessels. Macrophage RCT was markedly impaired in both models, even at sites with a leaky vasculature. Inhibited RCT was downstream of cholesterol efflux from macrophages, since macrophage efflux of a fluorescent cholesterol analog (BODIPY-cholesterol) was not altered by impaired lymphatic drainage. We next addressed whether RCT was mediated by lymphatic vessels from the aortic wall by loading the aortae of donor atherosclerotic <italic>Apoe</italic>
-deficient mice with [<sup>2</sup>
H]<sub>6</sub>
-labeled cholesterol and surgically transplanting these aortae into recipient <italic>Apoe</italic>
-deficient mice that were treated with anti-VEGFR3 antibody to block lymphatic regrowth or with control antibody to allow such regrowth. [<sup>2</sup>
H]-Cholesterol was retained in aortae of anti–VEGFR3-treated mice. Thus, the lymphatic vessel route is critical for RCT from multiple tissues, including the aortic wall. These results suggest that supporting lymphatic transport function may facilitate cholesterol clearance in therapies aimed at reversing atherosclerosis.
</p>
</div>
</front>
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<front><journal-meta><journal-id journal-id-type="nlm-ta">J Clin Invest</journal-id>
<journal-id journal-id-type="iso-abbrev">J. Clin. Invest</journal-id>
<journal-id journal-id-type="publisher-id">J CLIN INVEST</journal-id>
<journal-title-group><journal-title>The Journal of Clinical Investigation</journal-title>
</journal-title-group>
<issn pub-type="ppub">0021-9738</issn>
<issn pub-type="epub">1558-8238</issn>
<publisher><publisher-name>American Society for Clinical Investigation</publisher-name>
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<article-id pub-id-type="pmc">3613904</article-id>
<article-id pub-id-type="publisher-id">63685</article-id>
<article-id pub-id-type="doi">10.1172/JCI63685</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>Lymphatic vasculature mediates macrophage reverse cholesterol transport in mice</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Martel</surname>
<given-names>Catherine</given-names>
</name>
<xref ref-type="aff" rid="JCI63685">1</xref>
<xref ref-type="aff" rid="JCI63685">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Li</surname>
<given-names>Wenjun</given-names>
</name>
<xref ref-type="aff" rid="JCI63685">3</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Fulp</surname>
<given-names>Brian</given-names>
</name>
<xref ref-type="aff" rid="JCI63685">4</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Platt</surname>
<given-names>Andrew M.</given-names>
</name>
<xref ref-type="aff" rid="JCI63685">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Gautier</surname>
<given-names>Emmanuel L.</given-names>
</name>
<xref ref-type="aff" rid="JCI63685">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Westerterp</surname>
<given-names>Marit</given-names>
</name>
<xref ref-type="aff" rid="JCI63685">5</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Bittman</surname>
<given-names>Robert</given-names>
</name>
<xref ref-type="aff" rid="JCI63685">6</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Tall</surname>
<given-names>Alan R.</given-names>
</name>
<xref ref-type="aff" rid="JCI63685">5</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Chen</surname>
<given-names>Shu-Hsia</given-names>
</name>
<xref ref-type="aff" rid="JCI63685">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Thomas</surname>
<given-names>Michael J.</given-names>
</name>
<xref ref-type="aff" rid="JCI63685">7</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Kreisel</surname>
<given-names>Daniel</given-names>
</name>
<xref ref-type="aff" rid="JCI63685">2</xref>
<xref ref-type="aff" rid="JCI63685">3</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Swartz</surname>
<given-names>Melody A.</given-names>
</name>
<xref ref-type="aff" rid="JCI63685">8</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Sorci-Thomas</surname>
<given-names>Mary G.</given-names>
</name>
<xref ref-type="aff" rid="JCI63685">4</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Randolph</surname>
<given-names>Gwendalyn J.</given-names>
</name>
<xref ref-type="aff" rid="JCI63685">1</xref>
<xref ref-type="aff" rid="JCI63685">2</xref>
</contrib>
</contrib-group>
<aff id="JCI63685"><label>1</label>
Department of Gene and Cell Medicine, Mount Sinai School of Medicine, New York, New York, USA.<label>2</label>
Department of Pathology and<label>3</label>
Department of Surgery, Washington University, St. Louis, Missouri, USA.<label>4</label>
Department of Pathology, Wake Forest School of Medicine, Winston-Salem, North Carolina, USA.<label>5</label>
Department of Medicine, Columbia University, New York, New York, USA.<label>6</label>
Department of Chemistry and Biochemistry, Queens College of CUNY, Flushing, New York, USA.<label>7</label>
Department of Biochemistry, Wake Forest School of Medicine, Winston-Salem, North Carolina, USA.<label>8</label>
ωcole Polytechnique Fédérale de Lausanne, Lausanne, Switzerland.</aff>
<author-notes><corresp>Address correspondence to: Gwendalyn J. Randolph, Department of Pathology and Immunology, Washington University in St. Louis, 660 South Euclid Avenue, Campus Box 8118, St. Louis, Missouri 63110, USA. Phone: 314.286.2345; Fax: 314.362.9108; E-mail:
<email>grandolph@path.wustl.edu</email>
.
</corresp>
</author-notes>
<pub-date pub-type="epub"><day>25</day>
<month>3</month>
<year>2013</year>
</pub-date>
<pub-date pub-type="ppub"><day>1</day>
<month>4</month>
<year>2013</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>25</day>
<month>3</month>
<year>2013</year>
</pub-date>
<pmc-comment> PMC Release delay is 0 months and 0 days and was based on the
. </pmc-comment>
<volume>123</volume>
<issue>4</issue>
<fpage>1571</fpage>
<lpage>1579</lpage>
<history><date date-type="received"><day>4</day>
<month>12</month>
<year>2012</year>
</date>
<date date-type="accepted"><day>3</day>
<month>1</month>
<year>2013</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2013, American Society for Clinical Investigation</copyright-statement>
<copyright-year>2013</copyright-year>
</permissions>
<abstract><p>Reverse cholesterol transport (RCT) refers to the mobilization of cholesterol on HDL particles (HDL-C) from extravascular tissues to plasma, ultimately for fecal excretion. Little is known about how HDL-C leaves peripheral tissues to reach plasma. We first used 2 models of disrupted lymphatic drainage from skin — 1 surgical and the other genetic — to quantitatively track RCT following injection of [<sup>3</sup>
H]-cholesterol–loaded macrophages upstream of blocked or absent lymphatic vessels. Macrophage RCT was markedly impaired in both models, even at sites with a leaky vasculature. Inhibited RCT was downstream of cholesterol efflux from macrophages, since macrophage efflux of a fluorescent cholesterol analog (BODIPY-cholesterol) was not altered by impaired lymphatic drainage. We next addressed whether RCT was mediated by lymphatic vessels from the aortic wall by loading the aortae of donor atherosclerotic <italic>Apoe</italic>
-deficient mice with [<sup>2</sup>
H]<sub>6</sub>
-labeled cholesterol and surgically transplanting these aortae into recipient <italic>Apoe</italic>
-deficient mice that were treated with anti-VEGFR3 antibody to block lymphatic regrowth or with control antibody to allow such regrowth. [<sup>2</sup>
H]-Cholesterol was retained in aortae of anti–VEGFR3-treated mice. Thus, the lymphatic vessel route is critical for RCT from multiple tissues, including the aortic wall. These results suggest that supporting lymphatic transport function may facilitate cholesterol clearance in therapies aimed at reversing atherosclerosis.
</p>
</abstract>
</article-meta>
</front>
</pmc>
</record>
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