Segregated Foxc2, NFATc1 and Connexin expression at normal developing venous valves, and Connexin-specific differences in the valve phenotypes of Cx37, Cx43, and Cx47 knockout mice.
Identifieur interne : 000955 ( PubMed/Corpus ); précédent : 000954; suivant : 000956Segregated Foxc2, NFATc1 and Connexin expression at normal developing venous valves, and Connexin-specific differences in the valve phenotypes of Cx37, Cx43, and Cx47 knockout mice.
Auteurs : Stephanie J. Munger ; Xin Geng ; R Sathish Srinivasan ; Marlys H. Witte ; David L. Paul ; Alexander M. SimonSource :
- Developmental biology [ 1095-564X ] ; 2016.
English descriptors
- KwdEn :
- Animals, Connexin 43 (genetics), Connexin 43 (metabolism), Connexins (genetics), Connexins (metabolism), Forkhead Transcription Factors (genetics), Forkhead Transcription Factors (metabolism), Immunohistochemistry, Mice, Inbred C57BL, Mice, Knockout, NFATC Transcription Factors (genetics), NFATC Transcription Factors (metabolism), Phenotype, Time Factors, Venous Valves (embryology), Venous Valves (growth & development), Venous Valves (metabolism).
- MESH :
- chemical , genetics : Connexin 43, Connexins, Forkhead Transcription Factors, NFATC Transcription Factors.
- chemical , metabolism : Connexin 43, Connexins, Forkhead Transcription Factors, NFATC Transcription Factors.
- embryology : Venous Valves.
- growth & development : Venous Valves.
- metabolism : Venous Valves.
- Animals, Immunohistochemistry, Mice, Inbred C57BL, Mice, Knockout, Phenotype, Time Factors.
Abstract
Venous valves (VVs) are critical for unidirectional blood flow from superficial and deep veins towards the heart. Congenital valve aplasia or agenesis may, in some cases, be a direct cause of vascular disease, motivating an understanding of the molecular mechanisms underlying the development and maintenance of VVs. Three gap junction proteins (Connexins), Cx37, Cx43, and Cx47, are specifically expressed at VVs in a highly polarized fashion. VVs are absent from adult mice lacking Cx37; however it is not known if Cx37 is required for the initial formation of valves. In addition, the requirement of Cx43 and Cx47 for VV development has not been studied. Here, we provide a detailed description of Cx37, Cx43, and Cx47 expression during mouse vein development and show by gene knockout that each Cx is necessary for normal valve development. The valve phenotypes in the knockout lines exhibit Cx-specific differences, however, including whether peripheral or central VVs are affected by gene inactivation. In addition, we show that a Cx47 null mutation impairs peripheral VV development but does not affect lymphatic valve formation, a finding of significance for understanding how some CX47 mutations cause inherited lymphedema in humans. Finally, we demonstrate a striking segregation of Foxc2 and NFATc1 transcription factor expression between the downstream and upstream faces, respectively, of developing VV leaflets and show that this segregation is closely associated with the highly polarized expression of Cx37, Cx43, and Cx47. The partition of Foxc2 and NFATc1 expression at VV leaflets makes it unlikely that these factors directly cooperate during the leaflet elongation stage of VV development.
DOI: 10.1016/j.ydbio.2016.02.033
PubMed: 26953188
Links to Exploration step
pubmed:26953188Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Segregated Foxc2, NFATc1 and Connexin expression at normal developing venous valves, and Connexin-specific differences in the valve phenotypes of Cx37, Cx43, and Cx47 knockout mice.</title><author><name sortKey="Munger, Stephanie J" sort="Munger, Stephanie J" uniqKey="Munger S" first="Stephanie J" last="Munger">Stephanie J. Munger</name><affiliation><nlm:affiliation>Department of Physiology, University of Arizona, Tucson, AZ 85724, USA. Electronic address: sjmunger@email.arizona.edu.</nlm:affiliation></affiliation></author><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. Electronic address: Xin-geng@omrf.org.</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. Electronic address: Sathish-Srinivasan@omrf.org.</nlm:affiliation></affiliation></author><author><name sortKey="Witte, Marlys H" sort="Witte, Marlys H" uniqKey="Witte M" first="Marlys H" last="Witte">Marlys H. Witte</name><affiliation><nlm:affiliation>Department of Surgery, University of Arizona, Tucson, AZ 85724, USA. Electronic address: grace@surgery.arizona.edu.</nlm:affiliation></affiliation></author><author><name sortKey="Paul, David L" sort="Paul, David L" uniqKey="Paul D" first="David L" last="Paul">David L. Paul</name><affiliation><nlm:affiliation>Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA. Electronic address: dpaul@hms.harvard.edu.</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 85724, USA. 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Electronic address: sjmunger@email.arizona.edu.</nlm:affiliation></affiliation></author><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. Electronic address: Xin-geng@omrf.org.</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. Electronic address: Sathish-Srinivasan@omrf.org.</nlm:affiliation></affiliation></author><author><name sortKey="Witte, Marlys H" sort="Witte, Marlys H" uniqKey="Witte M" first="Marlys H" last="Witte">Marlys H. Witte</name><affiliation><nlm:affiliation>Department of Surgery, University of Arizona, Tucson, AZ 85724, USA. Electronic address: grace@surgery.arizona.edu.</nlm:affiliation></affiliation></author><author><name sortKey="Paul, David L" sort="Paul, David L" uniqKey="Paul D" first="David L" last="Paul">David L. Paul</name><affiliation><nlm:affiliation>Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA. Electronic address: dpaul@hms.harvard.edu.</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 85724, USA. Electronic address: amsimon@email.arizona.edu.</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>Connexin 43 (genetics)</term><term>Connexin 43 (metabolism)</term><term>Connexins (genetics)</term><term>Connexins (metabolism)</term><term>Forkhead Transcription Factors (genetics)</term><term>Forkhead Transcription Factors (metabolism)</term><term>Immunohistochemistry</term><term>Mice, Inbred C57BL</term><term>Mice, Knockout</term><term>NFATC Transcription Factors (genetics)</term><term>NFATC Transcription Factors (metabolism)</term><term>Phenotype</term><term>Time Factors</term><term>Venous Valves (embryology)</term><term>Venous Valves (growth & development)</term><term>Venous Valves (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Connexin 43</term><term>Connexins</term><term>Forkhead Transcription Factors</term><term>NFATC Transcription Factors</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Connexin 43</term><term>Connexins</term><term>Forkhead Transcription Factors</term><term>NFATC Transcription Factors</term></keywords><keywords scheme="MESH" qualifier="embryology" xml:lang="en"><term>Venous Valves</term></keywords><keywords scheme="MESH" qualifier="growth & development" xml:lang="en"><term>Venous Valves</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Venous Valves</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Immunohistochemistry</term><term>Mice, Inbred C57BL</term><term>Mice, Knockout</term><term>Phenotype</term><term>Time Factors</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Venous valves (VVs) are critical for unidirectional blood flow from superficial and deep veins towards the heart. Congenital valve aplasia or agenesis may, in some cases, be a direct cause of vascular disease, motivating an understanding of the molecular mechanisms underlying the development and maintenance of VVs. Three gap junction proteins (Connexins), Cx37, Cx43, and Cx47, are specifically expressed at VVs in a highly polarized fashion. VVs are absent from adult mice lacking Cx37; however it is not known if Cx37 is required for the initial formation of valves. In addition, the requirement of Cx43 and Cx47 for VV development has not been studied. Here, we provide a detailed description of Cx37, Cx43, and Cx47 expression during mouse vein development and show by gene knockout that each Cx is necessary for normal valve development. The valve phenotypes in the knockout lines exhibit Cx-specific differences, however, including whether peripheral or central VVs are affected by gene inactivation. In addition, we show that a Cx47 null mutation impairs peripheral VV development but does not affect lymphatic valve formation, a finding of significance for understanding how some CX47 mutations cause inherited lymphedema in humans. Finally, we demonstrate a striking segregation of Foxc2 and NFATc1 transcription factor expression between the downstream and upstream faces, respectively, of developing VV leaflets and show that this segregation is closely associated with the highly polarized expression of Cx37, Cx43, and Cx47. The partition of Foxc2 and NFATc1 expression at VV leaflets makes it unlikely that these factors directly cooperate during the leaflet elongation stage of VV development.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26953188</PMID><DateCreated><Year>2016</Year><Month>04</Month><Day>09</Day></DateCreated><DateCompleted><Year>2016</Year><Month>09</Month><Day>06</Day></DateCompleted><DateRevised><Year>2017</Year><Month>04</Month><Day>15</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1095-564X</ISSN><JournalIssue CitedMedium="Internet"><Volume>412</Volume><Issue>2</Issue><PubDate><Year>2016</Year><Month>Apr</Month><Day>15</Day></PubDate></JournalIssue><Title>Developmental biology</Title><ISOAbbreviation>Dev. Biol.</ISOAbbreviation></Journal><ArticleTitle>Segregated Foxc2, NFATc1 and Connexin expression at normal developing venous valves, and Connexin-specific differences in the valve phenotypes of Cx37, Cx43, and Cx47 knockout mice.</ArticleTitle><Pagination><MedlinePgn>173-90</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.ydbio.2016.02.033</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0012-1606(15)30258-X</ELocationID><Abstract><AbstractText>Venous valves (VVs) are critical for unidirectional blood flow from superficial and deep veins towards the heart. Congenital valve aplasia or agenesis may, in some cases, be a direct cause of vascular disease, motivating an understanding of the molecular mechanisms underlying the development and maintenance of VVs. Three gap junction proteins (Connexins), Cx37, Cx43, and Cx47, are specifically expressed at VVs in a highly polarized fashion. VVs are absent from adult mice lacking Cx37; however it is not known if Cx37 is required for the initial formation of valves. In addition, the requirement of Cx43 and Cx47 for VV development has not been studied. Here, we provide a detailed description of Cx37, Cx43, and Cx47 expression during mouse vein development and show by gene knockout that each Cx is necessary for normal valve development. The valve phenotypes in the knockout lines exhibit Cx-specific differences, however, including whether peripheral or central VVs are affected by gene inactivation. In addition, we show that a Cx47 null mutation impairs peripheral VV development but does not affect lymphatic valve formation, a finding of significance for understanding how some CX47 mutations cause inherited lymphedema in humans. Finally, we demonstrate a striking segregation of Foxc2 and NFATc1 transcription factor expression between the downstream and upstream faces, respectively, of developing VV leaflets and show that this segregation is closely associated with the highly polarized expression of Cx37, Cx43, and Cx47. The partition of Foxc2 and NFATc1 expression at VV leaflets makes it unlikely that these factors directly cooperate during the leaflet elongation stage of VV development.</AbstractText><CopyrightInformation>Copyright © 2016 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Munger</LastName><ForeName>Stephanie J</ForeName><Initials>SJ</Initials><AffiliationInfo><Affiliation>Department of Physiology, University of Arizona, Tucson, AZ 85724, USA. Electronic address: sjmunger@email.arizona.edu.</Affiliation></AffiliationInfo></Author><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. Electronic address: Xin-geng@omrf.org.</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. Electronic address: Sathish-Srinivasan@omrf.org.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Witte</LastName><ForeName>Marlys H</ForeName><Initials>MH</Initials><AffiliationInfo><Affiliation>Department of Surgery, University of Arizona, Tucson, AZ 85724, USA. Electronic address: grace@surgery.arizona.edu.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Paul</LastName><ForeName>David L</ForeName><Initials>DL</Initials><AffiliationInfo><Affiliation>Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA. Electronic address: dpaul@hms.harvard.edu.</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 85724, USA. Electronic address: amsimon@email.arizona.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 HL064232</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R21 HL122443</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01-HL64232</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R21-HL122443</GrantID><Acronym>HL</Acronym><Agency>NHLBI 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>2016</Year><Month>03</Month><Day>04</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Dev Biol</MedlineTA><NlmUniqueID>0372762</NlmUniqueID><ISSNLinking>0012-1606</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018031">Connexin 43</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D017630">Connexins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051858">Forkhead Transcription Factors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050778">NFATC Transcription Factors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C080179">connexin 37</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C427305">connexin 47</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C082078">mesenchyme fork head 1 protein</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Mol Cell Neurosci. 2007 Apr;34(4):629-41</RefSource><PMID Version="1">17344063</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Biochim Biophys Acta. 2013 Jan;1828(1):51-68</RefSource><PMID Version="1">22342665</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Cell Sci. 2003 Jun 1;116(Pt 11):2223-36</RefSource><PMID Version="1">12697838</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cardiovasc Res. 2010 Jul 1;87(1):166-76</RefSource><PMID Version="1">20110337</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurosci. 2003 Jul 2;23(13):5963-73</RefSource><PMID 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UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017630" MajorTopicYN="N">Connexins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051858" MajorTopicYN="N">Forkhead Transcription Factors</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007150" MajorTopicYN="N">Immunohistochemistry</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D050778" MajorTopicYN="N">NFATC Transcription Factors</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010641" MajorTopicYN="N">Phenotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013997" MajorTopicYN="N">Time Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D055422" MajorTopicYN="N">Venous Valves</DescriptorName><QualifierName UI="Q000196" MajorTopicYN="N">embryology</QualifierName><QualifierName UI="Q000254" MajorTopicYN="N">growth & development</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">NIHMS766122 [Available on 04/15/17]</OtherID><OtherID Source="NLM">PMC4826804 [Available on 04/15/17]</OtherID><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Chronic venous disease</Keyword><Keyword MajorTopicYN="N">Connexin</Keyword><Keyword MajorTopicYN="N">Foxc2</Keyword><Keyword MajorTopicYN="N">Lymphedema</Keyword><Keyword MajorTopicYN="N">NFATc1</Keyword><Keyword MajorTopicYN="N">Valve development</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>10</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2016</Year><Month>02</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>02</Month><Day>12</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>3</Month><Day>9</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>3</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>9</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">26953188</ArticleId><ArticleId IdType="pii">S0012-1606(15)30258-X</ArticleId><ArticleId IdType="doi">10.1016/j.ydbio.2016.02.033</ArticleId><ArticleId IdType="pmc">PMC4826804</ArticleId><ArticleId IdType="mid">NIHMS766122</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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|texte= Segregated Foxc2, NFATc1 and Connexin expression at normal developing venous valves, and Connexin-specific differences in the valve phenotypes of Cx37, Cx43, and Cx47 knockout mice.
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