Foxc1 and Foxc2 deletion causes abnormal lymphangiogenesis and correlates with ERK hyperactivation.
Identifieur interne : 000901 ( PubMed/Checkpoint ); précédent : 000900; suivant : 000902Foxc1 and Foxc2 deletion causes abnormal lymphangiogenesis and correlates with ERK hyperactivation.
Auteurs : Anees Fatima ; Ying Wang ; Yutaka Uchida ; Pieter Norden ; Ting Liu ; Austin Culver ; William H. Dietz ; Ford Culver ; Meredith Millay ; Yoh-Suke Mukouyama ; Tsutomu KumeSource :
- The Journal of clinical investigation [ 1558-8238 ] ; 2016.
Abstract
The lymphatic vasculature is essential for maintaining interstitial fluid homeostasis, and dysfunctional lymphangiogenesis contributes to various pathological processes, including inflammatory disease and tumor metastasis. Mutations in FOXC2 are dominantly associated with late-onset lymphedema; however, the precise role of FOXC2 and a closely related factor, FOXC1, in the lymphatic system remains largely unknown. Here we identified a molecular cascade by which FOXC1 and FOXC2 regulate ERK signaling in lymphatic vessel growth. In mice, lymphatic endothelial cell-specific (LEC-specific) deletion of Foxc1, Foxc2, or both resulted in increased LEC proliferation, enlarged lymphatic vessels, and abnormal lymphatic vessel morphogenesis. Compared with LECs from control animals, LECs from mice lacking both Foxc1 and Foxc2 exhibited aberrant expression of Ras regulators, and embryos with LEC-specific deletion of Foxc1 and Foxc2, alone or in combination, exhibited ERK hyperactivation. Pharmacological ERK inhibition in utero abolished the abnormally enlarged lymphatic vessels in FOXC-deficient embryos. Together, these results identify FOXC1 and FOXC2 as essential regulators of lymphangiogenesis and indicate a new potential mechanistic basis for lymphatic-associated diseases.
DOI: 10.1172/JCI80465
PubMed: 27214551
Affiliations:
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Dietz</name></author><author><name sortKey="Culver, Ford" sort="Culver, Ford" uniqKey="Culver F" first="Ford" last="Culver">Ford Culver</name></author><author><name sortKey="Millay, Meredith" sort="Millay, Meredith" uniqKey="Millay M" first="Meredith" last="Millay">Meredith Millay</name></author><author><name sortKey="Mukouyama, Yoh Suke" sort="Mukouyama, Yoh Suke" uniqKey="Mukouyama Y" first="Yoh-Suke" last="Mukouyama">Yoh-Suke Mukouyama</name></author><author><name sortKey="Kume, Tsutomu" sort="Kume, Tsutomu" uniqKey="Kume T" first="Tsutomu" last="Kume">Tsutomu Kume</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2016">2016</date><idno type="RBID">pubmed:27214551</idno><idno type="pmid">27214551</idno><idno type="doi">10.1172/JCI80465</idno><idno type="wicri:Area/PubMed/Corpus">000812</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000812</idno><idno type="wicri:Area/PubMed/Curation">000812</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000812</idno><idno type="wicri:Area/PubMed/Checkpoint">000812</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000812</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Foxc1 and Foxc2 deletion causes abnormal lymphangiogenesis and correlates with ERK hyperactivation.</title><author><name sortKey="Fatima, Anees" sort="Fatima, Anees" uniqKey="Fatima A" first="Anees" last="Fatima">Anees Fatima</name></author><author><name sortKey="Wang, Ying" sort="Wang, Ying" uniqKey="Wang Y" first="Ying" last="Wang">Ying Wang</name></author><author><name sortKey="Uchida, Yutaka" sort="Uchida, Yutaka" uniqKey="Uchida Y" first="Yutaka" last="Uchida">Yutaka Uchida</name></author><author><name sortKey="Norden, Pieter" sort="Norden, Pieter" uniqKey="Norden P" first="Pieter" last="Norden">Pieter Norden</name></author><author><name sortKey="Liu, Ting" sort="Liu, Ting" uniqKey="Liu T" first="Ting" last="Liu">Ting Liu</name></author><author><name sortKey="Culver, Austin" sort="Culver, Austin" uniqKey="Culver A" first="Austin" last="Culver">Austin Culver</name></author><author><name sortKey="Dietz, William H" sort="Dietz, William H" uniqKey="Dietz W" first="William H" last="Dietz">William H. Dietz</name></author><author><name sortKey="Culver, Ford" sort="Culver, Ford" uniqKey="Culver F" first="Ford" last="Culver">Ford Culver</name></author><author><name sortKey="Millay, Meredith" sort="Millay, Meredith" uniqKey="Millay M" first="Meredith" last="Millay">Meredith Millay</name></author><author><name sortKey="Mukouyama, Yoh Suke" sort="Mukouyama, Yoh Suke" uniqKey="Mukouyama Y" first="Yoh-Suke" last="Mukouyama">Yoh-Suke Mukouyama</name></author><author><name sortKey="Kume, Tsutomu" sort="Kume, Tsutomu" uniqKey="Kume T" first="Tsutomu" last="Kume">Tsutomu Kume</name></author></analytic><series><title level="j">The Journal of clinical investigation</title><idno type="eISSN">1558-8238</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The lymphatic vasculature is essential for maintaining interstitial fluid homeostasis, and dysfunctional lymphangiogenesis contributes to various pathological processes, including inflammatory disease and tumor metastasis. Mutations in FOXC2 are dominantly associated with late-onset lymphedema; however, the precise role of FOXC2 and a closely related factor, FOXC1, in the lymphatic system remains largely unknown. Here we identified a molecular cascade by which FOXC1 and FOXC2 regulate ERK signaling in lymphatic vessel growth. In mice, lymphatic endothelial cell-specific (LEC-specific) deletion of Foxc1, Foxc2, or both resulted in increased LEC proliferation, enlarged lymphatic vessels, and abnormal lymphatic vessel morphogenesis. Compared with LECs from control animals, LECs from mice lacking both Foxc1 and Foxc2 exhibited aberrant expression of Ras regulators, and embryos with LEC-specific deletion of Foxc1 and Foxc2, alone or in combination, exhibited ERK hyperactivation. Pharmacological ERK inhibition in utero abolished the abnormally enlarged lymphatic vessels in FOXC-deficient embryos. Together, these results identify FOXC1 and FOXC2 as essential regulators of lymphangiogenesis and indicate a new potential mechanistic basis for lymphatic-associated diseases.</div></front></TEI><pubmed><MedlineCitation Status="In-Process" Owner="NLM"><PMID Version="1">27214551</PMID><DateCreated><Year>2016</Year><Month>07</Month><Day>02</Day></DateCreated><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1558-8238</ISSN><JournalIssue CitedMedium="Internet"><Volume>126</Volume><Issue>7</Issue><PubDate><Year>2016</Year><Month>Jul</Month><Day>01</Day></PubDate></JournalIssue><Title>The Journal of clinical investigation</Title><ISOAbbreviation>J. Clin. Invest.</ISOAbbreviation></Journal><ArticleTitle>Foxc1 and Foxc2 deletion causes abnormal lymphangiogenesis and correlates with ERK hyperactivation.</ArticleTitle><Pagination><MedlinePgn>2437-51</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1172/JCI80465</ELocationID><ELocationID EIdType="pii" ValidYN="Y">80465</ELocationID><Abstract><AbstractText>The lymphatic vasculature is essential for maintaining interstitial fluid homeostasis, and dysfunctional lymphangiogenesis contributes to various pathological processes, including inflammatory disease and tumor metastasis. Mutations in FOXC2 are dominantly associated with late-onset lymphedema; however, the precise role of FOXC2 and a closely related factor, FOXC1, in the lymphatic system remains largely unknown. Here we identified a molecular cascade by which FOXC1 and FOXC2 regulate ERK signaling in lymphatic vessel growth. In mice, lymphatic endothelial cell-specific (LEC-specific) deletion of Foxc1, Foxc2, or both resulted in increased LEC proliferation, enlarged lymphatic vessels, and abnormal lymphatic vessel morphogenesis. Compared with LECs from control animals, LECs from mice lacking both Foxc1 and Foxc2 exhibited aberrant expression of Ras regulators, and embryos with LEC-specific deletion of Foxc1 and Foxc2, alone or in combination, exhibited ERK hyperactivation. Pharmacological ERK inhibition in utero abolished the abnormally enlarged lymphatic vessels in FOXC-deficient embryos. Together, these results identify FOXC1 and FOXC2 as essential regulators of lymphangiogenesis and indicate a new potential mechanistic basis for lymphatic-associated diseases.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Fatima</LastName><ForeName>Anees</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Ying</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Uchida</LastName><ForeName>Yutaka</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Norden</LastName><ForeName>Pieter</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Liu</LastName><ForeName>Ting</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Culver</LastName><ForeName>Austin</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Dietz</LastName><ForeName>William H</ForeName><Initials>WH</Initials></Author><Author ValidYN="Y"><LastName>Culver</LastName><ForeName>Ford</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Millay</LastName><ForeName>Meredith</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Mukouyama</LastName><ForeName>Yoh-Suke</ForeName><Initials>YS</Initials></Author><Author ValidYN="Y"><LastName>Kume</LastName><ForeName>Tsutomu</ForeName><Initials>T</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>AHA_14POST20390029</GrantID><Acronym>AHA</Acronym><Agency>None</Agency><Country>None</Country></Grant><Grant><GrantID>P30 CA060553</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 EY019484</GrantID><Acronym>EY</Acronym><Agency>NEI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL126920</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>05</Month><Day>23</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Clin Invest</MedlineTA><NlmUniqueID>7802877</NlmUniqueID><ISSNLinking>0021-9738</ISSNLinking></MedlineJournalInfo><CitationSubset>AIM</CitationSubset><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>J Clin Invest. 2015 Oct 1;125(10):3861-77</RefSource><PMID Version="1">26389677</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Mol Cell Biol. 2013 Oct;33(19):3749-61</RefSource><PMID Version="1">23878394</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Clin Invest. 2014 Mar;124(3):898-904</RefSource><PMID 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Dietz</name><name sortKey="Fatima, Anees" sort="Fatima, Anees" uniqKey="Fatima A" first="Anees" last="Fatima">Anees Fatima</name><name sortKey="Kume, Tsutomu" sort="Kume, Tsutomu" uniqKey="Kume T" first="Tsutomu" last="Kume">Tsutomu Kume</name><name sortKey="Liu, Ting" sort="Liu, Ting" uniqKey="Liu T" first="Ting" last="Liu">Ting Liu</name><name sortKey="Millay, Meredith" sort="Millay, Meredith" uniqKey="Millay M" first="Meredith" last="Millay">Meredith Millay</name><name sortKey="Mukouyama, Yoh Suke" sort="Mukouyama, Yoh Suke" uniqKey="Mukouyama Y" first="Yoh-Suke" last="Mukouyama">Yoh-Suke Mukouyama</name><name sortKey="Norden, Pieter" sort="Norden, Pieter" uniqKey="Norden P" first="Pieter" last="Norden">Pieter Norden</name><name sortKey="Uchida, Yutaka" sort="Uchida, Yutaka" uniqKey="Uchida Y" first="Yutaka" last="Uchida">Yutaka Uchida</name><name sortKey="Wang, Ying" sort="Wang, Ying" uniqKey="Wang Y" first="Ying" last="Wang">Ying Wang</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Checkpoint/biblio.hfd \
| NlmPubMed2Wicri -a LymphedemaV1
| This area was generated with Dilib version V0.6.31. |  |