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Cilostazol improves lymphatic function by inducing proliferation and stabilization of lymphatic endothelial cells.

Identifieur interne : 006285 ( Ncbi/Merge ); précédent : 006284; suivant : 006286

Cilostazol improves lymphatic function by inducing proliferation and stabilization of lymphatic endothelial cells.

Auteurs : Takayuki Kimura [Japon] ; Tatsuo S. Hamazaki [Japon] ; Makoto Sugaya [Japon] ; Shoji Fukuda [Japon] ; Techuan Chan [Japon] ; Miwa Tamura-Nakano [Japon] ; Shinichi Sato [Japon] ; Hitoshi Okochi [Japon]

Source :

RBID : pubmed:24517869

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English descriptors

Abstract

Cilostazol, an inhibitor of phosphodiesterase type III, is an antiplatelet agent and vasodilator. Some clinical reports have suggested that this drug can improve progressive and refractory lymphedema.

DOI: 10.1016/j.jdermsci.2014.01.001
PubMed: 24517869

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pubmed:24517869

Le document en format XML

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<term>Animals</term>
<term>Cell Movement (drug effects)</term>
<term>Cell Proliferation (drug effects)</term>
<term>Cells, Cultured</term>
<term>Disease Models, Animal</term>
<term>Drug Evaluation, Preclinical</term>
<term>Endothelial Cells (drug effects)</term>
<term>Endothelium, Lymphatic (drug effects)</term>
<term>Humans</term>
<term>Lymphangiogenesis (drug effects)</term>
<term>Lymphedema (drug therapy)</term>
<term>Mice</term>
<term>Mice, Transgenic</term>
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<term>Tetrazoles (pharmacology)</term>
<term>Tetrazoles (therapeutic use)</term>
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<term>Animaux</term>
<term>Cellules cultivées</term>
<term>Cellules endothéliales ()</term>
<term>Endothélium lymphatique ()</term>
<term>Humains</term>
<term>Inhibiteurs de la phosphodiestérase-3 (pharmacologie)</term>
<term>Inhibiteurs de la phosphodiestérase-3 (usage thérapeutique)</term>
<term>Lymphangiogenèse ()</term>
<term>Lymphoedème (traitement médicamenteux)</term>
<term>Modèles animaux de maladie humaine</term>
<term>Mouvement cellulaire ()</term>
<term>Prolifération cellulaire ()</term>
<term>Souris</term>
<term>Souris transgéniques</term>
<term>Tétrazoles (pharmacologie)</term>
<term>Tétrazoles (usage thérapeutique)</term>
<term>Évaluation préclinique de médicament</term>
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<term>Phosphodiesterase 3 Inhibitors</term>
<term>Tetrazoles</term>
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<term>Cell Movement</term>
<term>Cell Proliferation</term>
<term>Endothelial Cells</term>
<term>Endothelium, Lymphatic</term>
<term>Lymphangiogenesis</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en">
<term>Lymphedema</term>
</keywords>
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<term>Inhibiteurs de la phosphodiestérase-3</term>
<term>Tétrazoles</term>
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<term>Phosphodiesterase 3 Inhibitors</term>
<term>Tetrazoles</term>
</keywords>
<keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr">
<term>Lymphoedème</term>
</keywords>
<keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr">
<term>Inhibiteurs de la phosphodiestérase-3</term>
<term>Tétrazoles</term>
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<term>Mice</term>
<term>Mice, Transgenic</term>
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<term>Animaux</term>
<term>Cellules cultivées</term>
<term>Cellules endothéliales</term>
<term>Endothélium lymphatique</term>
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<term>Mouvement cellulaire</term>
<term>Prolifération cellulaire</term>
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<front>
<div type="abstract" xml:lang="en">Cilostazol, an inhibitor of phosphodiesterase type III, is an antiplatelet agent and vasodilator. Some clinical reports have suggested that this drug can improve progressive and refractory lymphedema.</div>
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<DateCreated>
<Year>2014</Year>
<Month>04</Month>
<Day>02</Day>
</DateCreated>
<DateCompleted>
<Year>2014</Year>
<Month>12</Month>
<Day>09</Day>
</DateCompleted>
<DateRevised>
<Year>2014</Year>
<Month>04</Month>
<Day>02</Day>
</DateRevised>
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<Journal>
<ISSN IssnType="Electronic">1873-569X</ISSN>
<JournalIssue CitedMedium="Internet">
<Volume>74</Volume>
<Issue>2</Issue>
<PubDate>
<Year>2014</Year>
<Month>May</Month>
</PubDate>
</JournalIssue>
<Title>Journal of dermatological science</Title>
<ISOAbbreviation>J. Dermatol. Sci.</ISOAbbreviation>
</Journal>
<ArticleTitle>Cilostazol improves lymphatic function by inducing proliferation and stabilization of lymphatic endothelial cells.</ArticleTitle>
<Pagination>
<MedlinePgn>150-8</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1016/j.jdermsci.2014.01.001</ELocationID>
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<Abstract>
<AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Cilostazol, an inhibitor of phosphodiesterase type III, is an antiplatelet agent and vasodilator. Some clinical reports have suggested that this drug can improve progressive and refractory lymphedema.</AbstractText>
<AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">In this study, we investigated whether cilostazol has the potential to proliferate lymphatic vessels and to improve lymphatic function using human lymphatic endothelial cells (LECs) and mouse lymphedema models.</AbstractText>
<AbstractText Label="METHODS" NlmCategory="METHODS">Human LECs were counted at several time points while they were cultured in the presence of cilostazol and/or protein kinase A inhibitor. After receiving a diet including 0.1% cilostazol or control diet, skin tissue and lymphatic function of k-cyclin transgenic (kCYC(+/-)) mice, which have pernicious lymphatic dysfunction, was analyzed. A different lymphedema model was generated in wild type mice by excising circumferential tail skin to remove the superficial lymphatics. After oral administration of cilostazol, tail lymphedema was examined in this mouse model.</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="RESULTS">Proliferation of LECs was promoted in a dose-dependent manner, which was partially inhibited by a protein kinase A inhibitor. Lymphatic vessel count increased in the cilostazol-treated kCYC(+/-) mice over that in the non-treated mice. Lymph flow improved in cilostazol-fed kCYC(+/-) mice as assessed by subcutaneous injection of Evans blue dye into the footpad. Oral administration of cilostazol also decreased lymphedema in a tail of wild type mice.</AbstractText>
<AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">Cilostazol promoted growth of human LECs and improved lymph flow and lymphedema in two different mouse lymphedema models. These results suggest that cilostazol would be a promising agent for the treatment of lymphedema.</AbstractText>
<CopyrightInformation>Copyright © 2014 Japanese Society for Investigative Dermatology. Published by Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation>
</Abstract>
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<LastName>Kimura</LastName>
<ForeName>Takayuki</ForeName>
<Initials>T</Initials>
<AffiliationInfo>
<Affiliation>Department of Regenerative Medicine, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan; Department of Dermatology, Faculty of Medicine, The University of Tokyo, Tokyo, Japan.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Hamazaki</LastName>
<ForeName>Tatsuo S</ForeName>
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<Affiliation>Department of Regenerative Medicine, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan. Electronic address: hamazaki@ri.ncgm.go.jp.</Affiliation>
</AffiliationInfo>
</Author>
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<LastName>Sugaya</LastName>
<ForeName>Makoto</ForeName>
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<AffiliationInfo>
<Affiliation>Department of Regenerative Medicine, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan; Department of Dermatology, Faculty of Medicine, The University of Tokyo, Tokyo, Japan.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Fukuda</LastName>
<ForeName>Shoji</ForeName>
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<AffiliationInfo>
<Affiliation>Department of Cardiovascular Surgery, National Center for Global Health and Medicine, Tokyo, Japan.</Affiliation>
</AffiliationInfo>
</Author>
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<LastName>Chan</LastName>
<ForeName>Techuan</ForeName>
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<AffiliationInfo>
<Affiliation>Department of Regenerative Medicine, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.</Affiliation>
</AffiliationInfo>
</Author>
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<LastName>Tamura-Nakano</LastName>
<ForeName>Miwa</ForeName>
<Initials>M</Initials>
<AffiliationInfo>
<Affiliation>EM Support Unit, National Center for Global Health and Medicine, Tokyo, Japan.</Affiliation>
</AffiliationInfo>
</Author>
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<LastName>Sato</LastName>
<ForeName>Shinichi</ForeName>
<Initials>S</Initials>
<AffiliationInfo>
<Affiliation>Department of Dermatology, Faculty of Medicine, The University of Tokyo, Tokyo, Japan.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Okochi</LastName>
<ForeName>Hitoshi</ForeName>
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<AffiliationInfo>
<Affiliation>Department of Regenerative Medicine, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.</Affiliation>
</AffiliationInfo>
</Author>
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<Language>eng</Language>
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<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
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<ArticleDate DateType="Electronic">
<Year>2014</Year>
<Month>01</Month>
<Day>21</Day>
</ArticleDate>
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<MedlineJournalInfo>
<Country>Netherlands</Country>
<MedlineTA>J Dermatol Sci</MedlineTA>
<NlmUniqueID>9011485</NlmUniqueID>
<ISSNLinking>0923-1811</ISSNLinking>
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<NameOfSubstance UI="D058987">Phosphodiesterase 3 Inhibitors</NameOfSubstance>
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<Chemical>
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<MeshHeading>
<DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D002465" MajorTopicYN="N">Cell Movement</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D004353" MajorTopicYN="N">Drug Evaluation, Preclinical</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D042783" MajorTopicYN="N">Endothelial Cells</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D004729" MajorTopicYN="N">Endothelium, Lymphatic</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D042583" MajorTopicYN="N">Lymphangiogenesis</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D008209" MajorTopicYN="N">Lymphedema</DescriptorName>
<QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D008822" MajorTopicYN="N">Mice, Transgenic</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D058987" MajorTopicYN="N">Phosphodiesterase 3 Inhibitors</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
<QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName>
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<DescriptorName UI="D013777" MajorTopicYN="N">Tetrazoles</DescriptorName>
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<QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM">
<Keyword MajorTopicYN="N">Cilostazol</Keyword>
<Keyword MajorTopicYN="N">Lymphatic endothelial cells</Keyword>
<Keyword MajorTopicYN="N">Lymphedema</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData>
<History>
<PubMedPubDate PubStatus="received">
<Year>2013</Year>
<Month>09</Month>
<Day>11</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised">
<Year>2013</Year>
<Month>12</Month>
<Day>25</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted">
<Year>2014</Year>
<Month>01</Month>
<Day>06</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez">
<Year>2014</Year>
<Month>2</Month>
<Day>13</Day>
<Hour>6</Hour>
<Minute>0</Minute>
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<PubMedPubDate PubStatus="pubmed">
<Year>2014</Year>
<Month>2</Month>
<Day>13</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline">
<Year>2014</Year>
<Month>12</Month>
<Day>15</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList>
<ArticleId IdType="pubmed">24517869</ArticleId>
<ArticleId IdType="pii">S0923-1811(14)00006-1</ArticleId>
<ArticleId IdType="doi">10.1016/j.jdermsci.2014.01.001</ArticleId>
</ArticleIdList>
</PubmedData>
</pubmed>
<affiliations>
<list>
<country>
<li>Japon</li>
</country>
<region>
<li>Région de Kantō</li>
</region>
<settlement>
<li>Tokyo</li>
</settlement>
<orgName>
<li>Université de Tokyo</li>
</orgName>
</list>
<tree>
<country name="Japon">
<region name="Région de Kantō">
<name sortKey="Kimura, Takayuki" sort="Kimura, Takayuki" uniqKey="Kimura T" first="Takayuki" last="Kimura">Takayuki Kimura</name>
</region>
<name sortKey="Chan, Techuan" sort="Chan, Techuan" uniqKey="Chan T" first="Techuan" last="Chan">Techuan Chan</name>
<name sortKey="Fukuda, Shoji" sort="Fukuda, Shoji" uniqKey="Fukuda S" first="Shoji" last="Fukuda">Shoji Fukuda</name>
<name sortKey="Hamazaki, Tatsuo S" sort="Hamazaki, Tatsuo S" uniqKey="Hamazaki T" first="Tatsuo S" last="Hamazaki">Tatsuo S. Hamazaki</name>
<name sortKey="Okochi, Hitoshi" sort="Okochi, Hitoshi" uniqKey="Okochi H" first="Hitoshi" last="Okochi">Hitoshi Okochi</name>
<name sortKey="Sato, Shinichi" sort="Sato, Shinichi" uniqKey="Sato S" first="Shinichi" last="Sato">Shinichi Sato</name>
<name sortKey="Sugaya, Makoto" sort="Sugaya, Makoto" uniqKey="Sugaya M" first="Makoto" last="Sugaya">Makoto Sugaya</name>
<name sortKey="Tamura Nakano, Miwa" sort="Tamura Nakano, Miwa" uniqKey="Tamura Nakano M" first="Miwa" last="Tamura-Nakano">Miwa Tamura-Nakano</name>
</country>
</tree>
</affiliations>
</record>

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