Foxc2 influences alveolar epithelial cell differentiation during lung development.
Identifieur interne : 000120 ( PubMed/Curation ); précédent : 000119; suivant : 000121Foxc2 influences alveolar epithelial cell differentiation during lung development.
Auteurs : Mayoko Tsuji [Japon] ; Masae Morishima [Japon] ; Kazuhiko Shimizu [Japon] ; Shunichi Morikawa [Japon] ; Mikael Heglind [Suède] ; Sven Enerb Ck [Suède] ; Taichi Ezaki [Japon] ; Jun Tamaoki [Japon]Source :
- Development, growth & differentiation [ 1440-169X ] ; 2017.
Abstract
FOXC2, a forkhead transcriptional factor, is a candidate gene for congenital heart diseases and lymphedema-distichiasis syndrome and yellow nail syndrome; however, there are no reports on Foxc2 and the development of the lung. We have identified lung abnormalities in Foxc2-knockout embryos during investigation of cardiac development. The aim of this study was to clarify the morphological characteristics during lung development using ICR-Foxc2 knockout lungs. Mutant fetuses at embryonic days 10.5-18.5 were obtained from mating of Foxc2(+/-) mice and then analyzed. Notably, Foxc2-knockout lungs appeared parenchymatous and much smaller than those of the wild-type littermates. In the Foxc2 knockout lungs, the capillary beds remained distant from the alveolar epithelium until the late stages, the number of type2 alveolar cells per alveolar progenitor cell was lower and the type1 alveolar cells were thicker in Foxc2 knockout mice. In contrast, Foxc2 expression was only detected in the mesenchyme of the lung buds at E10.5, and it disappeared at E11.5 in Foxc2-LacZ knockin mice. Furthermore, the expression of Lef1 was significantly inhibited in E11.5 lungs. All of these results suggest that the abnormalities in Foxc2 knockout mice may involve maldifferentiation of alveolar epithelial cells and capillary vessel endothelial-alveolar epithelial approach as well as lymph vessel malformation. This is the first report about relationship between Foxc2 and lung development. This animal model might provide an important clue for elucidating the mechanism of lung development and the cause of respiratory diseases.
DOI: 10.1111/dgd.12368
PubMed: 28675425
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xml:lang="fr">Japon</country><wicri:regionArea>Department of Anatomy and Developmental Biology, Tokyo Women's Medical University, Tokyo</wicri:regionArea></affiliation></author><author><name sortKey="Morikawa, Shunichi" sort="Morikawa, Shunichi" uniqKey="Morikawa S" first="Shunichi" last="Morikawa">Shunichi Morikawa</name><affiliation wicri:level="1"><nlm:affiliation>Department of Anatomy and Developmental Biology, Tokyo Women's Medical University, Tokyo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Anatomy and Developmental Biology, Tokyo Women's Medical University, Tokyo</wicri:regionArea></affiliation></author><author><name sortKey="Heglind, Mikael" sort="Heglind, Mikael" uniqKey="Heglind M" first="Mikael" last="Heglind">Mikael Heglind</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medical Biochemistry and Cell Biology, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden.</nlm:affiliation><country xml:lang="fr">Suède</country><wicri:regionArea>Department of Medical Biochemistry and Cell Biology, Institute of Biomedicine, University of Gothenburg, Gothenburg</wicri:regionArea></affiliation></author><author><name sortKey="Enerb Ck, Sven" sort="Enerb Ck, Sven" uniqKey="Enerb Ck S" first="Sven" last="Enerb Ck">Sven Enerb Ck</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medical Biochemistry and Cell Biology, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden.</nlm:affiliation><country xml:lang="fr">Suède</country><wicri:regionArea>Department of Medical Biochemistry and Cell Biology, Institute of Biomedicine, University of Gothenburg, Gothenburg</wicri:regionArea></affiliation></author><author><name sortKey="Ezaki, Taichi" sort="Ezaki, Taichi" uniqKey="Ezaki T" first="Taichi" last="Ezaki">Taichi Ezaki</name><affiliation wicri:level="1"><nlm:affiliation>Department of Anatomy and Developmental Biology, Tokyo Women's Medical University, Tokyo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Anatomy and Developmental Biology, Tokyo Women's Medical University, Tokyo</wicri:regionArea></affiliation></author><author><name sortKey="Tamaoki, Jun" sort="Tamaoki, Jun" uniqKey="Tamaoki J" first="Jun" last="Tamaoki">Jun Tamaoki</name><affiliation wicri:level="1"><nlm:affiliation>First Department of Medicine, Tokyo Women's Medical University, Tokyo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>First Department of Medicine, Tokyo Women's Medical University, Tokyo</wicri:regionArea></affiliation></author></analytic><series><title level="j">Development, growth & differentiation</title><idno type="eISSN">1440-169X</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">FOXC2, a forkhead transcriptional factor, is a candidate gene for congenital heart diseases and lymphedema-distichiasis syndrome and yellow nail syndrome; however, there are no reports on Foxc2 and the development of the lung. We have identified lung abnormalities in Foxc2-knockout embryos during investigation of cardiac development. The aim of this study was to clarify the morphological characteristics during lung development using ICR-Foxc2 knockout lungs. Mutant fetuses at embryonic days 10.5-18.5 were obtained from mating of Foxc2(+/-) mice and then analyzed. Notably, Foxc2-knockout lungs appeared parenchymatous and much smaller than those of the wild-type littermates. In the Foxc2 knockout lungs, the capillary beds remained distant from the alveolar epithelium until the late stages, the number of type2 alveolar cells per alveolar progenitor cell was lower and the type1 alveolar cells were thicker in Foxc2 knockout mice. In contrast, Foxc2 expression was only detected in the mesenchyme of the lung buds at E10.5, and it disappeared at E11.5 in Foxc2-LacZ knockin mice. Furthermore, the expression of Lef1 was significantly inhibited in E11.5 lungs. All of these results suggest that the abnormalities in Foxc2 knockout mice may involve maldifferentiation of alveolar epithelial cells and capillary vessel endothelial-alveolar epithelial approach as well as lymph vessel malformation. This is the first report about relationship between Foxc2 and lung development. This animal model might provide an important clue for elucidating the mechanism of lung development and the cause of respiratory diseases.</div></front></TEI><pubmed><MedlineCitation Status="In-Process" Owner="NLM"><PMID Version="1">28675425</PMID><DateCreated><Year>2017</Year><Month>07</Month><Day>04</Day></DateCreated><DateRevised><Year>2017</Year><Month>08</Month><Day>14</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1440-169X</ISSN><JournalIssue CitedMedium="Internet"><Volume>59</Volume><Issue>6</Issue><PubDate><Year>2017</Year><Month>Aug</Month></PubDate></JournalIssue><Title>Development, growth & differentiation</Title><ISOAbbreviation>Dev. Growth Differ.</ISOAbbreviation></Journal><ArticleTitle>Foxc2 influences alveolar epithelial cell differentiation during lung development.</ArticleTitle><Pagination><MedlinePgn>501-514</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/dgd.12368</ELocationID><Abstract><AbstractText>FOXC2, a forkhead transcriptional factor, is a candidate gene for congenital heart diseases and lymphedema-distichiasis syndrome and yellow nail syndrome; however, there are no reports on Foxc2 and the development of the lung. We have identified lung abnormalities in Foxc2-knockout embryos during investigation of cardiac development. The aim of this study was to clarify the morphological characteristics during lung development using ICR-Foxc2 knockout lungs. Mutant fetuses at embryonic days 10.5-18.5 were obtained from mating of Foxc2(+/-) mice and then analyzed. Notably, Foxc2-knockout lungs appeared parenchymatous and much smaller than those of the wild-type littermates. In the Foxc2 knockout lungs, the capillary beds remained distant from the alveolar epithelium until the late stages, the number of type2 alveolar cells per alveolar progenitor cell was lower and the type1 alveolar cells were thicker in Foxc2 knockout mice. In contrast, Foxc2 expression was only detected in the mesenchyme of the lung buds at E10.5, and it disappeared at E11.5 in Foxc2-LacZ knockin mice. Furthermore, the expression of Lef1 was significantly inhibited in E11.5 lungs. All of these results suggest that the abnormalities in Foxc2 knockout mice may involve maldifferentiation of alveolar epithelial cells and capillary vessel endothelial-alveolar epithelial approach as well as lymph vessel malformation. This is the first report about relationship between Foxc2 and lung development. This animal model might provide an important clue for elucidating the mechanism of lung development and the cause of respiratory diseases.</AbstractText><CopyrightInformation>© 2017 Japanese Society of Developmental Biologists.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tsuji</LastName><ForeName>Mayoko</ForeName><Initials>M</Initials><Identifier Source="ORCID">http://orcid.org/0000-0003-1526-7878</Identifier><AffiliationInfo><Affiliation>First Department of Medicine, Tokyo Women's Medical University, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Morishima</LastName><ForeName>Masae</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Anatomy and Developmental Biology, Tokyo Women's Medical University, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shimizu</LastName><ForeName>Kazuhiko</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Anatomy and Developmental Biology, Tokyo Women's Medical University, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Morikawa</LastName><ForeName>Shunichi</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Anatomy and Developmental Biology, Tokyo Women's Medical University, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Heglind</LastName><ForeName>Mikael</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Medical Biochemistry and Cell Biology, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Enerbäck</LastName><ForeName>Sven</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Medical Biochemistry and Cell Biology, Institute of Biomedicine, University of Gothenburg, Gothenburg, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ezaki</LastName><ForeName>Taichi</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Anatomy and Developmental Biology, Tokyo Women's Medical University, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tamaoki</LastName><ForeName>Jun</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>First Department of Medicine, Tokyo Women's Medical University, Tokyo, Japan.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>07</Month><Day>04</Day></ArticleDate></Article><MedlineJournalInfo><Country>Japan</Country><MedlineTA>Dev Growth Differ</MedlineTA><NlmUniqueID>0356504</NlmUniqueID><ISSNLinking>0012-1592</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Foxc2</Keyword><Keyword MajorTopicYN="N">Lef1</Keyword><Keyword MajorTopicYN="N">alveolar progenitor cell</Keyword><Keyword MajorTopicYN="N">lung development</Keyword><Keyword MajorTopicYN="N">mouse</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2017</Year><Month>01</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2017</Year><Month>04</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2017</Year><Month>05</Month><Day>07</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2017</Year><Month>7</Month><Day>5</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>7</Month><Day>5</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2017</Year><Month>7</Month><Day>5</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">28675425</ArticleId><ArticleId IdType="doi">10.1111/dgd.12368</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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