Multiple mouse models of primary lymphedema exhibit distinct defects in lymphovenous valve development.
Identifieur interne : 000B48 ( PubMed/Corpus ); précédent : 000B47; suivant : 000B49Multiple mouse models of primary lymphedema exhibit distinct defects in lymphovenous valve development.
Auteurs : Xin Geng ; Boksik Cha ; Md Riaj Mahamud ; Kim-Chew Lim ; Robert Silasi-Mansat ; Mohammad K M. Uddin ; Naoyuki Miura ; Lijun Xia ; Alexander M. Simon ; James Douglas Engel ; Hong Chen ; Florea Lupu ; R Sathish SrinivasanSource :
- Developmental biology [ 1095-564X ] ; 2016.
English descriptors
- KwdEn :
- Animals, Animals, Newborn, Cell Differentiation, Disease Models, Animal, Endothelial Cells (pathology), Endothelial Cells (ultrastructure), Lymphatic Vessels (embryology), Lymphatic Vessels (ultrastructure), Lymphedema (embryology), Lymphedema (pathology), Mice, Inbred C57BL, Morphogenesis, Penetrance, Phenotype, Venous Valves (embryology), Venous Valves (ultrastructure).
- MESH :
- embryology : Lymphatic Vessels, Lymphedema, Venous Valves.
- pathology : Endothelial Cells, Lymphedema.
- ultrastructure : Endothelial Cells, Lymphatic Vessels, Venous Valves.
- Animals, Animals, Newborn, Cell Differentiation, Disease Models, Animal, Mice, Inbred C57BL, Morphogenesis, Penetrance, Phenotype.
Abstract
Lymph is returned to the blood circulation exclusively via four lymphovenous valves (LVVs). Despite their vital importance, the architecture and development of LVVs is poorly understood. We analyzed the formation of LVVs at the molecular and ultrastructural levels during mouse embryogenesis and identified three critical steps. First, LVV-forming endothelial cells (LVV-ECs) differentiate from PROX1(+) progenitors and delaminate from the luminal side of the veins. Second, LVV-ECs aggregate, align perpendicular to the direction of lymph flow and establish lympho-venous connections. Finally, LVVs mature with the recruitment of mural cells. LVV morphogenesis is disrupted in four different mouse models of primary lymphedema and the severity of LVV defects correlate with that of lymphedema. In summary, we have provided the first and the most comprehensive analysis of LVV development. Furthermore, our work suggests that aberrant LVVs contribute to lymphedema.
DOI: 10.1016/j.ydbio.2015.10.022
PubMed: 26542011
Links to Exploration step
pubmed:26542011Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Multiple mouse models of primary lymphedema exhibit distinct defects in lymphovenous valve development.</title><author><name sortKey="Geng, Xin" sort="Geng, Xin" uniqKey="Geng X" first="Xin" last="Geng">Xin Geng</name><affiliation><nlm:affiliation>Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Cha, Boksik" sort="Cha, Boksik" uniqKey="Cha B" first="Boksik" last="Cha">Boksik Cha</name><affiliation><nlm:affiliation>Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Mahamud, Md Riaj" sort="Mahamud, Md Riaj" uniqKey="Mahamud M" first="Md Riaj" last="Mahamud">Md Riaj Mahamud</name><affiliation><nlm:affiliation>Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Lim, Kim Chew" sort="Lim, Kim Chew" uniqKey="Lim K" first="Kim-Chew" last="Lim">Kim-Chew Lim</name><affiliation><nlm:affiliation>Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, MI, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Silasi Mansat, Robert" sort="Silasi Mansat, Robert" uniqKey="Silasi Mansat R" first="Robert" last="Silasi-Mansat">Robert Silasi-Mansat</name><affiliation><nlm:affiliation>Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Uddin, Mohammad K M" sort="Uddin, Mohammad K M" uniqKey="Uddin M" first="Mohammad K M" last="Uddin">Mohammad K M. Uddin</name><affiliation><nlm:affiliation>Department of Biochemistry, Hamamatsu University School of Medicine, Hamamatsu, Japan.</nlm:affiliation></affiliation></author><author><name sortKey="Miura, Naoyuki" sort="Miura, Naoyuki" uniqKey="Miura N" first="Naoyuki" last="Miura">Naoyuki Miura</name><affiliation><nlm:affiliation>Department of Biochemistry, Hamamatsu University School of Medicine, Hamamatsu, Japan.</nlm:affiliation></affiliation></author><author><name sortKey="Xia, Lijun" sort="Xia, Lijun" uniqKey="Xia L" first="Lijun" last="Xia">Lijun Xia</name><affiliation><nlm:affiliation>Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Simon, Alexander M" sort="Simon, Alexander M" uniqKey="Simon A" first="Alexander M" last="Simon">Alexander M. Simon</name><affiliation><nlm:affiliation>Department of Physiology, University of Arizona, Tucson, AZ, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Engel, James Douglas" sort="Engel, James Douglas" uniqKey="Engel J" first="James Douglas" last="Engel">James Douglas Engel</name><affiliation><nlm:affiliation>Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, MI, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Chen, Hong" sort="Chen, Hong" uniqKey="Chen H" first="Hong" last="Chen">Hong Chen</name><affiliation><nlm:affiliation>Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Lupu, Florea" sort="Lupu, Florea" uniqKey="Lupu F" first="Florea" last="Lupu">Florea Lupu</name><affiliation><nlm:affiliation>Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Srinivasan, R Sathish" sort="Srinivasan, R Sathish" uniqKey="Srinivasan R" first="R Sathish" last="Srinivasan">R Sathish Srinivasan</name><affiliation><nlm:affiliation>Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA; Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA. Electronic address: sathish-srinivasan@omrf.org.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2016">2016</date><idno type="RBID">pubmed:26542011</idno><idno type="pmid">26542011</idno><idno type="doi">10.1016/j.ydbio.2015.10.022</idno><idno type="wicri:Area/PubMed/Corpus">000B48</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000B48</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Multiple mouse models of primary lymphedema exhibit distinct defects in lymphovenous valve development.</title><author><name sortKey="Geng, Xin" sort="Geng, Xin" uniqKey="Geng X" first="Xin" last="Geng">Xin Geng</name><affiliation><nlm:affiliation>Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Cha, Boksik" sort="Cha, Boksik" uniqKey="Cha B" first="Boksik" last="Cha">Boksik Cha</name><affiliation><nlm:affiliation>Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Mahamud, Md Riaj" sort="Mahamud, Md Riaj" uniqKey="Mahamud M" first="Md Riaj" last="Mahamud">Md Riaj Mahamud</name><affiliation><nlm:affiliation>Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Lim, Kim Chew" sort="Lim, Kim Chew" uniqKey="Lim K" first="Kim-Chew" last="Lim">Kim-Chew Lim</name><affiliation><nlm:affiliation>Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, MI, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Silasi Mansat, Robert" sort="Silasi Mansat, Robert" uniqKey="Silasi Mansat R" first="Robert" last="Silasi-Mansat">Robert Silasi-Mansat</name><affiliation><nlm:affiliation>Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Uddin, Mohammad K M" sort="Uddin, Mohammad K M" uniqKey="Uddin M" first="Mohammad K M" last="Uddin">Mohammad K M. Uddin</name><affiliation><nlm:affiliation>Department of Biochemistry, Hamamatsu University School of Medicine, Hamamatsu, Japan.</nlm:affiliation></affiliation></author><author><name sortKey="Miura, Naoyuki" sort="Miura, Naoyuki" uniqKey="Miura N" first="Naoyuki" last="Miura">Naoyuki Miura</name><affiliation><nlm:affiliation>Department of Biochemistry, Hamamatsu University School of Medicine, Hamamatsu, Japan.</nlm:affiliation></affiliation></author><author><name sortKey="Xia, Lijun" sort="Xia, Lijun" uniqKey="Xia L" first="Lijun" last="Xia">Lijun Xia</name><affiliation><nlm:affiliation>Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Simon, Alexander M" sort="Simon, Alexander M" uniqKey="Simon A" first="Alexander M" last="Simon">Alexander M. Simon</name><affiliation><nlm:affiliation>Department of Physiology, University of Arizona, Tucson, AZ, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Engel, James Douglas" sort="Engel, James Douglas" uniqKey="Engel J" first="James Douglas" last="Engel">James Douglas Engel</name><affiliation><nlm:affiliation>Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, MI, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Chen, Hong" sort="Chen, Hong" uniqKey="Chen H" first="Hong" last="Chen">Hong Chen</name><affiliation><nlm:affiliation>Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Lupu, Florea" sort="Lupu, Florea" uniqKey="Lupu F" first="Florea" last="Lupu">Florea Lupu</name><affiliation><nlm:affiliation>Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Srinivasan, R Sathish" sort="Srinivasan, R Sathish" uniqKey="Srinivasan R" first="R Sathish" last="Srinivasan">R Sathish Srinivasan</name><affiliation><nlm:affiliation>Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA; Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA. Electronic address: sathish-srinivasan@omrf.org.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Developmental biology</title><idno type="eISSN">1095-564X</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Animals, Newborn</term><term>Cell Differentiation</term><term>Disease Models, Animal</term><term>Endothelial Cells (pathology)</term><term>Endothelial Cells (ultrastructure)</term><term>Lymphatic Vessels (embryology)</term><term>Lymphatic Vessels (ultrastructure)</term><term>Lymphedema (embryology)</term><term>Lymphedema (pathology)</term><term>Mice, Inbred C57BL</term><term>Morphogenesis</term><term>Penetrance</term><term>Phenotype</term><term>Venous Valves (embryology)</term><term>Venous Valves (ultrastructure)</term></keywords><keywords scheme="MESH" qualifier="embryology" xml:lang="en"><term>Lymphatic Vessels</term><term>Lymphedema</term><term>Venous Valves</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Endothelial Cells</term><term>Lymphedema</term></keywords><keywords scheme="MESH" qualifier="ultrastructure" xml:lang="en"><term>Endothelial Cells</term><term>Lymphatic Vessels</term><term>Venous Valves</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Animals, Newborn</term><term>Cell Differentiation</term><term>Disease Models, Animal</term><term>Mice, Inbred C57BL</term><term>Morphogenesis</term><term>Penetrance</term><term>Phenotype</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Lymph is returned to the blood circulation exclusively via four lymphovenous valves (LVVs). Despite their vital importance, the architecture and development of LVVs is poorly understood. We analyzed the formation of LVVs at the molecular and ultrastructural levels during mouse embryogenesis and identified three critical steps. First, LVV-forming endothelial cells (LVV-ECs) differentiate from PROX1(+) progenitors and delaminate from the luminal side of the veins. Second, LVV-ECs aggregate, align perpendicular to the direction of lymph flow and establish lympho-venous connections. Finally, LVVs mature with the recruitment of mural cells. LVV morphogenesis is disrupted in four different mouse models of primary lymphedema and the severity of LVV defects correlate with that of lymphedema. In summary, we have provided the first and the most comprehensive analysis of LVV development. Furthermore, our work suggests that aberrant LVVs contribute to lymphedema.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26542011</PMID><DateCreated><Year>2015</Year><Month>12</Month><Day>21</Day></DateCreated><DateCompleted><Year>2016</Year><Month>05</Month><Day>25</Day></DateCompleted><DateRevised><Year>2017</Year><Month>01</Month><Day>01</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1095-564X</ISSN><JournalIssue CitedMedium="Internet"><Volume>409</Volume><Issue>1</Issue><PubDate><Year>2016</Year><Month>Jan</Month><Day>01</Day></PubDate></JournalIssue><Title>Developmental biology</Title><ISOAbbreviation>Dev. Biol.</ISOAbbreviation></Journal><ArticleTitle>Multiple mouse models of primary lymphedema exhibit distinct defects in lymphovenous valve development.</ArticleTitle><Pagination><MedlinePgn>218-33</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.ydbio.2015.10.022</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0012-1606(15)30103-2</ELocationID><Abstract><AbstractText>Lymph is returned to the blood circulation exclusively via four lymphovenous valves (LVVs). Despite their vital importance, the architecture and development of LVVs is poorly understood. We analyzed the formation of LVVs at the molecular and ultrastructural levels during mouse embryogenesis and identified three critical steps. First, LVV-forming endothelial cells (LVV-ECs) differentiate from PROX1(+) progenitors and delaminate from the luminal side of the veins. Second, LVV-ECs aggregate, align perpendicular to the direction of lymph flow and establish lympho-venous connections. Finally, LVVs mature with the recruitment of mural cells. LVV morphogenesis is disrupted in four different mouse models of primary lymphedema and the severity of LVV defects correlate with that of lymphedema. In summary, we have provided the first and the most comprehensive analysis of LVV development. Furthermore, our work suggests that aberrant LVVs contribute to lymphedema.</AbstractText><CopyrightInformation>Copyright © 2015 The Authors. Published by Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Geng</LastName><ForeName>Xin</ForeName><Initials>X</Initials><AffiliationInfo><Affiliation>Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cha</LastName><ForeName>Boksik</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mahamud</LastName><ForeName>Md Riaj</ForeName><Initials>MR</Initials><AffiliationInfo><Affiliation>Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lim</LastName><ForeName>Kim-Chew</ForeName><Initials>KC</Initials><AffiliationInfo><Affiliation>Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, MI, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Silasi-Mansat</LastName><ForeName>Robert</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Uddin</LastName><ForeName>Mohammad K M</ForeName><Initials>MK</Initials><AffiliationInfo><Affiliation>Department of Biochemistry, Hamamatsu University School of Medicine, Hamamatsu, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Miura</LastName><ForeName>Naoyuki</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Department of Biochemistry, Hamamatsu University School of Medicine, Hamamatsu, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xia</LastName><ForeName>Lijun</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Simon</LastName><ForeName>Alexander M</ForeName><Initials>AM</Initials><AffiliationInfo><Affiliation>Department of Physiology, University of Arizona, Tucson, AZ, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Engel</LastName><ForeName>James Douglas</ForeName><Initials>JD</Initials><AffiliationInfo><Affiliation>Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, MI, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Hong</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lupu</LastName><ForeName>Florea</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Srinivasan</LastName><ForeName>R Sathish</ForeName><Initials>RS</Initials><AffiliationInfo><Affiliation>Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA; Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA. Electronic address: sathish-srinivasan@omrf.org.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>P20 GM103441</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P20GM103441</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>11</Month><Day>02</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Dev 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Clin Invest. 2008 Nov;118(11):3725-37</RefSource><PMID Version="1">18924607</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000831" MajorTopicYN="N">Animals, Newborn</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002454" MajorTopicYN="N">Cell Differentiation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D042783" MajorTopicYN="N">Endothelial Cells</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000648" MajorTopicYN="N">ultrastructure</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D042601" MajorTopicYN="N">Lymphatic Vessels</DescriptorName><QualifierName UI="Q000196" MajorTopicYN="Y">embryology</QualifierName><QualifierName UI="Q000648" MajorTopicYN="N">ultrastructure</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008209" MajorTopicYN="N">Lymphedema</DescriptorName><QualifierName UI="Q000196" MajorTopicYN="Y">embryology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009024" MajorTopicYN="N">Morphogenesis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019683" MajorTopicYN="N">Penetrance</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010641" MajorTopicYN="N">Phenotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D055422" MajorTopicYN="N">Venous Valves</DescriptorName><QualifierName UI="Q000196" MajorTopicYN="Y">embryology</QualifierName><QualifierName UI="Q000648" MajorTopicYN="N">ultrastructure</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">NIHMS736429 [Available on 01/01/17]</OtherID><OtherID Source="NLM">PMC4688075 [Available on 01/01/17]</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>08</Month><Day>03</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2015</Year><Month>10</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2015</Year><Month>10</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>11</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>11</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>5</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">26542011</ArticleId><ArticleId IdType="pii">S0012-1606(15)30103-2</ArticleId><ArticleId IdType="doi">10.1016/j.ydbio.2015.10.022</ArticleId><ArticleId IdType="pmc">PMC4688075</ArticleId><ArticleId IdType="mid">NIHMS736429</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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