Abnormal lymphangiogenesis in idiopathic pulmonary fibrosis with insights into cellular and molecular mechanisms
Identifieur interne : 003161 ( Pmc/Curation ); précédent : 003160; suivant : 003162Abnormal lymphangiogenesis in idiopathic pulmonary fibrosis with insights into cellular and molecular mechanisms
Auteurs : Souheil El-Chemaly ; Daniela Malide ; Enrique Zudaire [États-Unis] ; Yoshihiko Ikeda ; Benjamin A. Weinberg ; Gustavo Pacheco-Rodriguez ; Ivan O. Rosas ; Marta Aparicio [États-Unis] ; Ping Ren ; Sandra D. Macdonald ; Hai-Ping Wu ; Steven D. Nathan [États-Unis] ; Frank Cuttitta [États-Unis] ; J. Philip Mccoy [États-Unis] ; Bernadette R. Gochuico [États-Unis] ; Joel MossSource :
- Proceedings of the National Academy of Sciences of the United States of America [ 0027-8424 ] ; 2009.
Abstract
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, debilitating respiratory disease whose pathogenesis is poorly understood. In IPF, the lung parenchyma undergoes extensive remodeling. We hypothesized that lymphangiogenesis is part of lung remodeling and sought to characterize pathways leading to lymphangiogenesis in IPF. We found that the diameter of lymphatic vessels in alveolar spaces in IPF lung tissue correlated with disease severity, suggesting that the alveolar microenvironment plays a role in the lymphangiogenic process. In bronchoalveolar lavage fluid (BALF) from subjects with IPF, we found short-fragment hyaluronic acid, which induced migration and proliferation of lymphatic endothelial cells (LECs), processes required for lymphatic vessel formation. To determine the origin of LECs in IPF, we isolated macrophages from the alveolar spaces; CD11b+ macrophages from subjects with IPF, but not those from healthy volunteers, formed lymphatic-like vessels in vitro. Our findings demonstrate that in the alveolar microenvironment of IPF, soluble factors such as short-fragment hyaluronic acid and cells such as CD11b+ macrophages contribute to lymphangiogenesis. These results improve our understanding of lymphangiogenesis and tissue remodeling in IPF and perhaps other fibrotic diseases as well.
Url:
DOI: 10.1073/pnas.0813368106
PubMed: 19237567
PubMed Central: 2646625
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Weinberg</name><affiliation><nlm:aff wicri:cut=", and" id="aff2">Light Microscopy Core Facility</nlm:aff></affiliation></author><author><name sortKey="Pacheco Rodriguez, Gustavo" sort="Pacheco Rodriguez, Gustavo" uniqKey="Pacheco Rodriguez G" first="Gustavo" last="Pacheco-Rodriguez">Gustavo Pacheco-Rodriguez</name><affiliation><nlm:aff id="aff1">Translational Medicine Branch,</nlm:aff></affiliation></author><author><name sortKey="Rosas, Ivan O" sort="Rosas, Ivan O" uniqKey="Rosas I" first="Ivan O." last="Rosas">Ivan O. Rosas</name><affiliation><nlm:aff id="aff1">Translational Medicine Branch,</nlm:aff></affiliation></author><author><name sortKey="Aparicio, Marta" sort="Aparicio, Marta" uniqKey="Aparicio M" first="Marta" last="Aparicio">Marta Aparicio</name><affiliation wicri:level="2"><nlm:aff id="aff4">Angiogenesis Core Facility, National Cancer Institute, National Institutes of Health, Gaithersburg, MD 20877;</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>Angiogenesis Core Facility, National Cancer Institute, National Institutes of Health, Gaithersburg</wicri:cityArea></affiliation></author><author><name sortKey="Ren, Ping" sort="Ren, Ping" uniqKey="Ren P" first="Ping" last="Ren">Ping Ren</name><affiliation><nlm:aff id="aff1">Translational Medicine Branch,</nlm:aff></affiliation></author><author><name sortKey="Macdonald, Sandra D" sort="Macdonald, Sandra D" uniqKey="Macdonald S" first="Sandra D." last="Macdonald">Sandra D. Macdonald</name><affiliation><nlm:aff id="aff1">Translational Medicine Branch,</nlm:aff></affiliation></author><author><name sortKey="Wu, Hai Ping" sort="Wu, Hai Ping" uniqKey="Wu H" first="Hai-Ping" last="Wu">Hai-Ping Wu</name><affiliation><nlm:aff id="aff1">Translational Medicine Branch,</nlm:aff></affiliation></author><author><name sortKey="Nathan, Steven D" sort="Nathan, Steven D" uniqKey="Nathan S" first="Steven D." last="Nathan">Steven D. Nathan</name><affiliation wicri:level="2"><nlm:aff wicri:cut="; and" id="aff5">Advanced Lung Disease and Transplant Program, Inova Heart & Vascular Institute, Inova Fairfax Hospital, Falls Church, VA 22042</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Virginie</region></placeName><wicri:cityArea>Advanced Lung Disease and Transplant Program, Inova Heart & Vascular Institute, Inova Fairfax Hospital, Falls Church</wicri:cityArea></affiliation></author><author><name sortKey="Cuttitta, Frank" sort="Cuttitta, Frank" uniqKey="Cuttitta F" first="Frank" last="Cuttitta">Frank Cuttitta</name><affiliation wicri:level="2"><nlm:aff id="aff4">Angiogenesis Core Facility, National Cancer Institute, National Institutes of Health, Gaithersburg, MD 20877;</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>Angiogenesis Core Facility, National Cancer Institute, National Institutes of Health, Gaithersburg</wicri:cityArea></affiliation></author><author><name sortKey="Mccoy, J Philip" sort="Mccoy, J Philip" uniqKey="Mccoy J" first="J. Philip" last="Mccoy">J. Philip Mccoy</name><affiliation wicri:level="2"><nlm:aff id="aff3">Flow Cytometry Core Facility, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892;</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>Flow Cytometry Core Facility, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda</wicri:cityArea></affiliation></author><author><name sortKey="Gochuico, Bernadette R" sort="Gochuico, Bernadette R" uniqKey="Gochuico B" first="Bernadette R." last="Gochuico">Bernadette R. Gochuico</name><affiliation wicri:level="2"><nlm:aff id="aff6">Medical Genetics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>Medical Genetics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda</wicri:cityArea></affiliation></author><author><name sortKey="Moss, Joel" sort="Moss, Joel" uniqKey="Moss J" first="Joel" last="Moss">Joel Moss</name><affiliation><nlm:aff id="aff1">Translational Medicine Branch,</nlm:aff></affiliation></author></analytic><series><title level="j">Proceedings of the National Academy of Sciences of the United States of America</title><idno type="ISSN">0027-8424</idno><idno type="eISSN">1091-6490</idno><imprint><date when="2009">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, debilitating respiratory disease whose pathogenesis is poorly understood. In IPF, the lung parenchyma undergoes extensive remodeling. We hypothesized that lymphangiogenesis is part of lung remodeling and sought to characterize pathways leading to lymphangiogenesis in IPF. We found that the diameter of lymphatic vessels in alveolar spaces in IPF lung tissue correlated with disease severity, suggesting that the alveolar microenvironment plays a role in the lymphangiogenic process. In bronchoalveolar lavage fluid (BALF) from subjects with IPF, we found short-fragment hyaluronic acid, which induced migration and proliferation of lymphatic endothelial cells (LECs), processes required for lymphatic vessel formation. To determine the origin of LECs in IPF, we isolated macrophages from the alveolar spaces; CD11b<sup>+</sup> macrophages from subjects with IPF, but not those from healthy volunteers, formed lymphatic-like vessels in vitro. Our findings demonstrate that in the alveolar microenvironment of IPF, soluble factors such as short-fragment hyaluronic acid and cells such as CD11b<sup>+</sup> macrophages contribute to lymphangiogenesis. These results improve our understanding of lymphangiogenesis and tissue remodeling in IPF and perhaps other fibrotic diseases as well.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Proc Natl Acad Sci U S A</journal-id><journal-id journal-id-type="hwp">pnas</journal-id><journal-id journal-id-type="pmc">pnas</journal-id><journal-id journal-id-type="publisher-id">PNAS</journal-id><journal-title-group><journal-title>Proceedings of the National Academy of Sciences of the United States of America</journal-title></journal-title-group><issn pub-type="ppub">0027-8424</issn><issn pub-type="epub">1091-6490</issn><publisher><publisher-name>National Academy of Sciences</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">19237567</article-id><article-id pub-id-type="pmc">2646625</article-id><article-id pub-id-type="publisher-id">6827</article-id><article-id pub-id-type="doi">10.1073/pnas.0813368106</article-id><article-categories><subj-group subj-group-type="heading"><subject>Biological Sciences</subject><subj-group><subject>Medical Sciences</subject></subj-group></subj-group></article-categories><title-group><article-title>Abnormal lymphangiogenesis in idiopathic pulmonary fibrosis with insights into cellular and molecular mechanisms</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>El-Chemaly</surname><given-names>Souheil</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author"><name><surname>Malide</surname><given-names>Daniela</given-names></name><xref ref-type="aff" rid="aff2"><sup>b</sup></xref></contrib><contrib contrib-type="author"><name><surname>Zudaire</surname><given-names>Enrique</given-names></name><xref ref-type="aff" rid="aff4"><sup>c</sup></xref></contrib><contrib contrib-type="author"><name><surname>Ikeda</surname><given-names>Yoshihiko</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref><xref ref-type="author-notes" rid="FN1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Weinberg</surname><given-names>Benjamin A.</given-names></name><xref ref-type="aff" rid="aff2"><sup>b</sup></xref></contrib><contrib contrib-type="author"><name><surname>Pacheco-Rodriguez</surname><given-names>Gustavo</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author"><name><surname>Rosas</surname><given-names>Ivan O.</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref><xref ref-type="author-notes" rid="FN2"><sup>2</sup></xref></contrib><contrib contrib-type="author"><name><surname>Aparicio</surname><given-names>Marta</given-names></name><xref ref-type="aff" rid="aff4"><sup>c</sup></xref></contrib><contrib contrib-type="author"><name><surname>Ren</surname><given-names>Ping</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author"><name><surname>MacDonald</surname><given-names>Sandra D.</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author"><name><surname>Wu</surname><given-names>Hai-Ping</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref></contrib><contrib contrib-type="author"><name><surname>Nathan</surname><given-names>Steven D.</given-names></name><xref ref-type="aff" rid="aff5"><sup>d</sup></xref></contrib><contrib contrib-type="author"><name><surname>Cuttitta</surname><given-names>Frank</given-names></name><xref ref-type="aff" rid="aff4"><sup>c</sup></xref></contrib><contrib contrib-type="author"><name><surname>McCoy</surname><given-names>J. Philip</given-names></name><xref ref-type="aff" rid="aff3"><sup>e</sup></xref></contrib><contrib contrib-type="author"><name><surname>Gochuico</surname><given-names>Bernadette R.</given-names></name><xref ref-type="aff" rid="aff6"><sup>f</sup></xref></contrib><contrib contrib-type="author"><name><surname>Moss</surname><given-names>Joel</given-names></name><xref ref-type="aff" rid="aff1"><sup>a</sup></xref><xref ref-type="corresp" rid="cor1"><sup>3</sup></xref></contrib><aff id="aff1"><sup>a</sup>Translational Medicine Branch,</aff><aff id="aff2"><sup>b</sup>Light Microscopy Core Facility, and</aff><aff id="aff3"><sup>e</sup>Flow Cytometry Core Facility, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892;</aff><aff id="aff4"><sup>c</sup>Angiogenesis Core Facility, National Cancer Institute, National Institutes of Health, Gaithersburg, MD 20877;</aff><aff id="aff5"><sup>d</sup>Advanced Lung Disease and Transplant Program, Inova Heart & Vascular Institute, Inova Fairfax Hospital, Falls Church, VA 22042; and</aff><aff id="aff6"><sup>f</sup>Medical Genetics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892</aff></contrib-group><author-notes><corresp id="cor1"><sup>3</sup>To whom correspondence should be addressed. E-mail: <email>mossj@nhlbi.nih.gov</email></corresp><fn fn-type="com"><p>Communicated by Martha Vaughan, National Heart, Lung, and Blood Institute, Bethesda, MD, December 31, 2008</p></fn><fn fn-type="con"><p>Author contributions: S.E.-C., D.M., E.Z., G.P.-R., B.R.G., and J.M. designed research; S.E.-C., D.M., E.Z., Y.I., M.A., S.D.M., F.C., J.P.M., and B.R.G. performed research; I.O.R., S.D.N., F.C., and B.R.G. contributed new reagents/analytic tools; S.E.-C., D.M., E.Z., B.A.W., G.P.-R., P.R., H.-P.W., J.P.M., and J.M. analyzed data; and S.E.-C., D.M., G.P.-R., B.R.G., and J.M. wrote the paper.</p></fn><fn id="FN1" fn-type="present-address"><p><sup>1</sup>Present address: Department of Pathology, National Cardiovascular Center 5–7-1, Fujishirodai, Suita, Osaka 565-8565, Japan.</p></fn><fn id="FN2" fn-type="present-address"><p><sup>2</sup>Present address: Department of Medicine, Division of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115.</p></fn></author-notes><pub-date pub-type="ppub"><day>10</day><month>3</month><year>2009</year></pub-date><pub-date pub-type="epub"><day>23</day><month>2</month><year>2009</year></pub-date><pub-date pub-type="pmc-release"><day>23</day><month>2</month><year>2009</year></pub-date><pmc-comment> PMC Release delay is 0 months and 0 days and was based on the
epub date downloaded from Highwire. </pmc-comment>
<volume>106</volume><issue>10</issue><fpage>3958</fpage><lpage>3963</lpage><history><date date-type="received"><day>1</day><month>12</month><year>2008</year></date></history><permissions><copyright-statement>© 2009 by The National Academy of Sciences of the USA</copyright-statement><license license-type="open-access"><license-p>Freely available online through the PNAS open access option.</license-p></license></permissions><self-uri xlink:title="pdf" xlink:type="simple" xlink:href="zpq01009003958.pdf"></self-uri><abstract><p>Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, debilitating respiratory disease whose pathogenesis is poorly understood. In IPF, the lung parenchyma undergoes extensive remodeling. We hypothesized that lymphangiogenesis is part of lung remodeling and sought to characterize pathways leading to lymphangiogenesis in IPF. We found that the diameter of lymphatic vessels in alveolar spaces in IPF lung tissue correlated with disease severity, suggesting that the alveolar microenvironment plays a role in the lymphangiogenic process. In bronchoalveolar lavage fluid (BALF) from subjects with IPF, we found short-fragment hyaluronic acid, which induced migration and proliferation of lymphatic endothelial cells (LECs), processes required for lymphatic vessel formation. To determine the origin of LECs in IPF, we isolated macrophages from the alveolar spaces; CD11b<sup>+</sup> macrophages from subjects with IPF, but not those from healthy volunteers, formed lymphatic-like vessels in vitro. Our findings demonstrate that in the alveolar microenvironment of IPF, soluble factors such as short-fragment hyaluronic acid and cells such as CD11b<sup>+</sup> macrophages contribute to lymphangiogenesis. These results improve our understanding of lymphangiogenesis and tissue remodeling in IPF and perhaps other fibrotic diseases as well.</p></abstract><kwd-group><kwd>endothelial cell</kwd><kwd>hyaluronan</kwd><kwd>idiopathic pulmonary fibrosis</kwd><kwd>lymphangiogenesis</kwd><kwd>macrophage</kwd></kwd-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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