Absence of venous valves in mice lacking Connexin37
Identifieur interne : 002B83 ( Pmc/Checkpoint ); précédent : 002B82; suivant : 002B84Absence of venous valves in mice lacking Connexin37
Auteurs : Stephanie J. Munger ; John D. Kanady ; Alexander M. SimonSource :
- Developmental biology [ 0012-1606 ] ; 2012.
Abstract
Venous valves play a crucial role in blood circulation, promoting the one-way movement of blood from superficial and deep veins towards the heart. By preventing retrograde flow, venous valves spare capillaries and venules from being subjected to damaging elevations in pressure, especially during skeletal muscle contraction. Pathologically, valvular incompetence or absence of valves are common features of venous disorders such as chronic venous insufficiency and varicose veins. The underlying causes of these conditions are not well understood, but congenital venous valve aplasia or agenesis may play a role in some cases. Despite progress in the study of cardiac and lymphatic valve morphogenesis, the molecular mechanisms controlling the development and maintenance of venous valves remain poorly understood. Here, we show that in valved veins of the mouse, three gap junction proteins (Connexins, Cxs), Cx37, Cx43, and Cx47, are expressed exclusively in the valves in a highly polarized fashion, with Cx43 on the upstream side of the valve leaflet and Cx37 on the downstream side. Surprisingly, Cx43 expression is strongly induced in the non-valve venous endothelium in superficial veins following wounding of the overlying skin. Moreover, we show that in Cx37-deficient mice, venous valves are entirely absent. Thus, Cx37, a protein involved in cell-cell communication, is one of only a few proteins identified so far as critical for the development or maintenance of venous valves. Because Cxs are necessary for the development of valves in lymphatic vessels as well, our results support the notion of common molecular pathways controlling valve development in veins and lymphatic vessels.
Url:
DOI: 10.1016/j.ydbio.2012.10.032
PubMed: 23142761
PubMed Central: 3533519
Affiliations:
Links toward previous steps (curation, corpus...)
Links to Exploration step
PMC:3533519Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Absence of venous valves in mice lacking Connexin37</title>
<author><name sortKey="Munger, Stephanie J" sort="Munger, Stephanie J" uniqKey="Munger S" first="Stephanie J." last="Munger">Stephanie J. Munger</name>
</author>
<author><name sortKey="Kanady, John D" sort="Kanady, John D" uniqKey="Kanady J" first="John D." last="Kanady">John D. Kanady</name>
</author>
<author><name sortKey="Simon, Alexander M" sort="Simon, Alexander M" uniqKey="Simon A" first="Alexander M." last="Simon">Alexander M. Simon</name>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PMC</idno>
<idno type="pmid">23142761</idno>
<idno type="pmc">3533519</idno>
<idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3533519</idno>
<idno type="RBID">PMC:3533519</idno>
<idno type="doi">10.1016/j.ydbio.2012.10.032</idno>
<date when="2012">2012</date>
<idno type="wicri:Area/Pmc/Corpus">003352</idno>
<idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">003352</idno>
<idno type="wicri:Area/Pmc/Curation">003351</idno>
<idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">003351</idno>
<idno type="wicri:Area/Pmc/Checkpoint">002B83</idno>
<idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">002B83</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Absence of venous valves in mice lacking Connexin37</title>
<author><name sortKey="Munger, Stephanie J" sort="Munger, Stephanie J" uniqKey="Munger S" first="Stephanie J." last="Munger">Stephanie J. Munger</name>
</author>
<author><name sortKey="Kanady, John D" sort="Kanady, John D" uniqKey="Kanady J" first="John D." last="Kanady">John D. Kanady</name>
</author>
<author><name sortKey="Simon, Alexander M" sort="Simon, Alexander M" uniqKey="Simon A" first="Alexander M." last="Simon">Alexander M. Simon</name>
</author>
</analytic>
<series><title level="j">Developmental biology</title>
<idno type="ISSN">0012-1606</idno>
<idno type="eISSN">1095-564X</idno>
<imprint><date when="2012">2012</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass></textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><p id="P1">Venous valves play a crucial role in blood circulation, promoting the one-way movement of blood from superficial and deep veins towards the heart. By preventing retrograde flow, venous valves spare capillaries and venules from being subjected to damaging elevations in pressure, especially during skeletal muscle contraction. Pathologically, valvular incompetence or absence of valves are common features of venous disorders such as chronic venous insufficiency and varicose veins. The underlying causes of these conditions are not well understood, but congenital venous valve aplasia or agenesis may play a role in some cases. Despite progress in the study of cardiac and lymphatic valve morphogenesis, the molecular mechanisms controlling the development and maintenance of venous valves remain poorly understood. Here, we show that in valved veins of the mouse, three gap junction proteins (Connexins, Cxs), Cx37, Cx43, and Cx47, are expressed exclusively in the valves in a highly polarized fashion, with Cx43 on the upstream side of the valve leaflet and Cx37 on the downstream side. Surprisingly, Cx43 expression is strongly induced in the non-valve venous endothelium in superficial veins following wounding of the overlying skin. Moreover, we show that in Cx37-deficient mice, venous valves are entirely absent. Thus, Cx37, a protein involved in cell-cell communication, is one of only a few proteins identified so far as critical for the development or maintenance of venous valves. Because Cxs are necessary for the development of valves in lymphatic vessels as well, our results support the notion of common molecular pathways controlling valve development in veins and lymphatic vessels.</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>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">0372762</journal-id>
<journal-id journal-id-type="pubmed-jr-id">3389</journal-id>
<journal-id journal-id-type="nlm-ta">Dev Biol</journal-id>
<journal-id journal-id-type="iso-abbrev">Dev. Biol.</journal-id>
<journal-title-group><journal-title>Developmental biology</journal-title>
</journal-title-group>
<issn pub-type="ppub">0012-1606</issn>
<issn pub-type="epub">1095-564X</issn>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">23142761</article-id>
<article-id pub-id-type="pmc">3533519</article-id>
<article-id pub-id-type="doi">10.1016/j.ydbio.2012.10.032</article-id>
<article-id pub-id-type="manuscript">NIHMS421343</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>Absence of venous valves in mice lacking Connexin37</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Munger</surname>
<given-names>Stephanie J.</given-names>
</name>
<email>sjmunger@email.arizona.edu</email>
</contrib>
<contrib contrib-type="author"><name><surname>Kanady</surname>
<given-names>John D.</given-names>
</name>
<email>jkanady@email.arizona.edu</email>
</contrib>
<contrib contrib-type="author"><name><surname>Simon</surname>
<given-names>Alexander M.</given-names>
</name>
<email>amsimon@email.arizona.edu</email>
<xref ref-type="corresp" rid="cor1">*</xref>
</contrib>
<aff id="A1">Department of Physiology, University of Arizona, Tucson, AZ 85724, USA</aff>
</contrib-group>
<author-notes><corresp id="cor1"><label>*</label>
Author for correspondence: Alexander M. Simon, Ph.D., Department of Physiology, University of Arizona, PO Box 245051, Tucson, AZ 85724, USA, Phone: 520-621-9778, Fax: 520-626-2383, <email>amsimon@email.arizona.edu</email>
</corresp>
</author-notes>
<pub-date pub-type="nihms-submitted"><day>16</day>
<month>11</month>
<year>2012</year>
</pub-date>
<pub-date pub-type="epub"><day>07</day>
<month>11</month>
<year>2012</year>
</pub-date>
<pub-date pub-type="ppub"><day>15</day>
<month>1</month>
<year>2013</year>
</pub-date>
<pub-date pub-type="pmc-release"><day>15</day>
<month>1</month>
<year>2014</year>
</pub-date>
<volume>373</volume>
<issue>2</issue>
<fpage>338</fpage>
<lpage>348</lpage>
<permissions><copyright-statement>© 2012 Elsevier Inc. All rights reserved.</copyright-statement>
<copyright-year>2012</copyright-year>
</permissions>
<abstract><p id="P1">Venous valves play a crucial role in blood circulation, promoting the one-way movement of blood from superficial and deep veins towards the heart. By preventing retrograde flow, venous valves spare capillaries and venules from being subjected to damaging elevations in pressure, especially during skeletal muscle contraction. Pathologically, valvular incompetence or absence of valves are common features of venous disorders such as chronic venous insufficiency and varicose veins. The underlying causes of these conditions are not well understood, but congenital venous valve aplasia or agenesis may play a role in some cases. Despite progress in the study of cardiac and lymphatic valve morphogenesis, the molecular mechanisms controlling the development and maintenance of venous valves remain poorly understood. Here, we show that in valved veins of the mouse, three gap junction proteins (Connexins, Cxs), Cx37, Cx43, and Cx47, are expressed exclusively in the valves in a highly polarized fashion, with Cx43 on the upstream side of the valve leaflet and Cx37 on the downstream side. Surprisingly, Cx43 expression is strongly induced in the non-valve venous endothelium in superficial veins following wounding of the overlying skin. Moreover, we show that in Cx37-deficient mice, venous valves are entirely absent. Thus, Cx37, a protein involved in cell-cell communication, is one of only a few proteins identified so far as critical for the development or maintenance of venous valves. Because Cxs are necessary for the development of valves in lymphatic vessels as well, our results support the notion of common molecular pathways controlling valve development in veins and lymphatic vessels.</p>
</abstract>
<kwd-group><kwd>connexin</kwd>
<kwd>Cx37</kwd>
<kwd>gap junction</kwd>
<kwd>venous valve</kwd>
<kwd>chronic venous disease</kwd>
<kwd>wound healing</kwd>
</kwd-group>
<funding-group><award-group><funding-source country="United States">National Heart, Lung, and Blood Institute : NHLBI</funding-source>
<award-id>T32 HL007249 || HL</award-id>
</award-group>
<award-group><funding-source country="United States">National Heart, Lung, and Blood Institute : NHLBI</funding-source>
<award-id>R01 HL064232 || HL</award-id>
</award-group>
</funding-group>
</article-meta>
</front>
</pmc>
<affiliations><list></list>
<tree><noCountry><name sortKey="Kanady, John D" sort="Kanady, John D" uniqKey="Kanady J" first="John D." last="Kanady">John D. Kanady</name>
<name sortKey="Munger, Stephanie J" sort="Munger, Stephanie J" uniqKey="Munger S" first="Stephanie J." last="Munger">Stephanie J. Munger</name>
<name sortKey="Simon, Alexander M" sort="Simon, Alexander M" uniqKey="Simon A" first="Alexander M." last="Simon">Alexander M. Simon</name>
</noCountry>
</tree>
</affiliations>
</record>
Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/LymphedemaV1/Data/Pmc/Checkpoint
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 002B83 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Pmc/Checkpoint/biblio.hfd -nk 002B83 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien |wiki= Wicri/Sante |area= LymphedemaV1 |flux= Pmc |étape= Checkpoint |type= RBID |clé= PMC:3533519 |texte= Absence of venous valves in mice lacking Connexin37 }}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Pmc/Checkpoint/RBID.i -Sk "pubmed:23142761" \ | HfdSelect -Kh $EXPLOR_AREA/Data/Pmc/Checkpoint/biblio.hfd \ | NlmPubMed2Wicri -a LymphedemaV1
![]() | This area was generated with Dilib version V0.6.31. | ![]() |