Lymphatic fate specification: an ERK-controlled transcriptional program.
Identifieur interne : 001456 ( PubMed/Checkpoint ); précédent : 001455; suivant : 001457Lymphatic fate specification: an ERK-controlled transcriptional program.
Auteurs : Pengchun Yu [États-Unis] ; Joe K. Tung [États-Unis] ; Michael Simons [États-Unis]Source :
- Microvascular research [ 1095-9319 ] ; 2014.
Descripteurs français
- KwdFr :
- Animaux, Extracellular Signal-Regulated MAP Kinases (métabolisme), Facteur de croissance endothéliale vasculaire de type A (métabolisme), Facteurs de transcription SOX-F (métabolisme), Humains, Lignage cellulaire, Lymphangiogenèse (physiologie), Modèles biologiques, Protéines suppresseurs de tumeurs (métabolisme), Protéines à homéodomaine (métabolisme), Récepteurs Notch (métabolisme), Souris, Transcription génétique, Transduction du signal, Vaisseaux lymphatiques (physiologie).
- MESH :
- métabolisme : Extracellular Signal-Regulated MAP Kinases, Facteur de croissance endothéliale vasculaire de type A, Facteurs de transcription SOX-F, Protéines suppresseurs de tumeurs, Protéines à homéodomaine, Récepteurs Notch.
- physiologie : Lymphangiogenèse, Vaisseaux lymphatiques.
- Animaux, Humains, Lignage cellulaire, Modèles biologiques, Souris, Transcription génétique, Transduction du signal.
English descriptors
- KwdEn :
- Animals, Cell Lineage, Extracellular Signal-Regulated MAP Kinases (metabolism), Homeodomain Proteins (metabolism), Humans, Lymphangiogenesis (physiology), Lymphatic Vessels (physiology), Mice, Models, Biological, Receptors, Notch (metabolism), SOXF Transcription Factors (metabolism), Signal Transduction, Transcription, Genetic, Tumor Suppressor Proteins (metabolism), Vascular Endothelial Growth Factor A (metabolism).
- MESH :
- chemical , metabolism : Extracellular Signal-Regulated MAP Kinases, Homeodomain Proteins, Receptors, Notch, SOXF Transcription Factors, Tumor Suppressor Proteins, Vascular Endothelial Growth Factor A.
- physiology : Lymphangiogenesis, Lymphatic Vessels.
- Animals, Cell Lineage, Humans, Mice, Models, Biological, Signal Transduction, Transcription, Genetic.
Abstract
Lymphatic vessels are intimately involved in the regulation of water and solute homeostasis by returning interstitial fluid back to the venous circulation and play an equally important role in immune responses by providing avenues for immune cell transport. Defects in the lymphatic vasculature result in a number of pathological conditions, including lymphedema and lymphangiectasia. Knowledge of molecular mechanisms underlying lymphatic development and maintenance is therefore critical for understanding, prevention and treatment of lymphatic circulation-related diseases. Research in the past two decades has uncovered several key transcriptional factors (Prox1, Sox18 and Coup-TFII) controlling lymphatic fate specification. Most recently, ERK signaling has emerged as a critical regulator of this transcriptional program. This review summarizes our current understanding of lymphatic fate determination and its transcriptional controls.
DOI: 10.1016/j.mvr.2014.07.016
PubMed: 25132472
Affiliations:
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Tung</name><affiliation wicri:level="2"><nlm:affiliation>Yale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, New Haven, CT 06520, United States.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Yale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, New Haven, CT 06520</wicri:regionArea><placeName><region type="state">Connecticut</region></placeName></affiliation></author><author><name sortKey="Simons, Michael" sort="Simons, Michael" uniqKey="Simons M" first="Michael" last="Simons">Michael Simons</name><affiliation wicri:level="2"><nlm:affiliation>Yale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, New Haven, CT 06520, United States; Department of Cell Biology, Yale University School of Medicine, New Haven, CT 06520, United States. Electronic address: michael.simons@yale.edu.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Yale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, New Haven, CT 06520, United States; Department of Cell Biology, Yale University School of Medicine, New Haven, CT 06520</wicri:regionArea><placeName><region type="state">Connecticut</region></placeName></affiliation></author></analytic><series><title level="j">Microvascular research</title><idno type="eISSN">1095-9319</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Cell Lineage</term><term>Extracellular Signal-Regulated MAP Kinases (metabolism)</term><term>Homeodomain Proteins (metabolism)</term><term>Humans</term><term>Lymphangiogenesis (physiology)</term><term>Lymphatic Vessels (physiology)</term><term>Mice</term><term>Models, Biological</term><term>Receptors, Notch (metabolism)</term><term>SOXF Transcription Factors (metabolism)</term><term>Signal Transduction</term><term>Transcription, Genetic</term><term>Tumor Suppressor Proteins (metabolism)</term><term>Vascular Endothelial Growth Factor A (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Extracellular Signal-Regulated MAP Kinases (métabolisme)</term><term>Facteur de croissance endothéliale vasculaire de type A (métabolisme)</term><term>Facteurs de transcription SOX-F (métabolisme)</term><term>Humains</term><term>Lignage cellulaire</term><term>Lymphangiogenèse (physiologie)</term><term>Modèles biologiques</term><term>Protéines suppresseurs de tumeurs (métabolisme)</term><term>Protéines à homéodomaine (métabolisme)</term><term>Récepteurs Notch (métabolisme)</term><term>Souris</term><term>Transcription génétique</term><term>Transduction du signal</term><term>Vaisseaux lymphatiques (physiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Extracellular Signal-Regulated MAP Kinases</term><term>Homeodomain Proteins</term><term>Receptors, Notch</term><term>SOXF Transcription Factors</term><term>Tumor Suppressor Proteins</term><term>Vascular Endothelial Growth Factor A</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Extracellular Signal-Regulated MAP Kinases</term><term>Facteur de croissance endothéliale vasculaire de type A</term><term>Facteurs de transcription SOX-F</term><term>Protéines suppresseurs de tumeurs</term><term>Protéines à homéodomaine</term><term>Récepteurs Notch</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Lymphangiogenèse</term><term>Vaisseaux lymphatiques</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Lymphangiogenesis</term><term>Lymphatic Vessels</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Lineage</term><term>Humans</term><term>Mice</term><term>Models, Biological</term><term>Signal Transduction</term><term>Transcription, Genetic</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Humains</term><term>Lignage cellulaire</term><term>Modèles biologiques</term><term>Souris</term><term>Transcription génétique</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Lymphatic vessels are intimately involved in the regulation of water and solute homeostasis by returning interstitial fluid back to the venous circulation and play an equally important role in immune responses by providing avenues for immune cell transport. Defects in the lymphatic vasculature result in a number of pathological conditions, including lymphedema and lymphangiectasia. Knowledge of molecular mechanisms underlying lymphatic development and maintenance is therefore critical for understanding, prevention and treatment of lymphatic circulation-related diseases. Research in the past two decades has uncovered several key transcriptional factors (Prox1, Sox18 and Coup-TFII) controlling lymphatic fate specification. Most recently, ERK signaling has emerged as a critical regulator of this transcriptional program. This review summarizes our current understanding of lymphatic fate determination and its transcriptional controls.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25132472</PMID><DateCreated><Year>2014</Year><Month>12</Month><Day>16</Day></DateCreated><DateCompleted><Year>2015</Year><Month>08</Month><Day>31</Day></DateCompleted><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1095-9319</ISSN><JournalIssue CitedMedium="Internet"><Volume>96</Volume><PubDate><Year>2014</Year><Month>Nov</Month></PubDate></JournalIssue><Title>Microvascular research</Title><ISOAbbreviation>Microvasc. Res.</ISOAbbreviation></Journal><ArticleTitle>Lymphatic fate specification: an ERK-controlled transcriptional program.</ArticleTitle><Pagination><MedlinePgn>10-5</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.mvr.2014.07.016</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0026-2862(14)00123-X</ELocationID><Abstract><AbstractText>Lymphatic vessels are intimately involved in the regulation of water and solute homeostasis by returning interstitial fluid back to the venous circulation and play an equally important role in immune responses by providing avenues for immune cell transport. Defects in the lymphatic vasculature result in a number of pathological conditions, including lymphedema and lymphangiectasia. Knowledge of molecular mechanisms underlying lymphatic development and maintenance is therefore critical for understanding, prevention and treatment of lymphatic circulation-related diseases. Research in the past two decades has uncovered several key transcriptional factors (Prox1, Sox18 and Coup-TFII) controlling lymphatic fate specification. Most recently, ERK signaling has emerged as a critical regulator of this transcriptional program. This review summarizes our current understanding of lymphatic fate determination and its transcriptional controls.</AbstractText><CopyrightInformation>Copyright © 2014 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Yu</LastName><ForeName>Pengchun</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Yale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, New Haven, CT 06520, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tung</LastName><ForeName>Joe K</ForeName><Initials>JK</Initials><AffiliationInfo><Affiliation>Yale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, New Haven, CT 06520, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Simons</LastName><ForeName>Michael</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Yale Cardiovascular Research Center, Section of Cardiovascular Medicine, Department of Internal Medicine, New Haven, CT 06520, United States; Department of Cell Biology, Yale University School of Medicine, New Haven, CT 06520, United States. Electronic address: michael.simons@yale.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 HL053793</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL084619</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>HL084619</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="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>08</Month><Day>15</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Microvasc 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Endothelial Growth Factor A</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">NIHMS623119</OtherID><OtherID Source="NLM">PMC4268409</OtherID><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">ERK</Keyword><Keyword MajorTopicYN="N">Lymphangiogenesis</Keyword><Keyword MajorTopicYN="N">Lymphatic fate</Keyword><Keyword MajorTopicYN="N">Prox1</Keyword><Keyword MajorTopicYN="N">Sox18</Keyword><Keyword MajorTopicYN="N">VEGF-C</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2014</Year><Month>05</Month><Day>01</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2014</Year><Month>07</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2014</Year><Month>07</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>8</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2014</Year><Month>8</Month><Day>19</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>9</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">25132472</ArticleId><ArticleId IdType="pii">S0026-2862(14)00123-X</ArticleId><ArticleId IdType="doi">10.1016/j.mvr.2014.07.016</ArticleId><ArticleId IdType="pmc">PMC4268409</ArticleId><ArticleId IdType="mid">NIHMS623119</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>Connecticut</li></region></list><tree><country name="États-Unis"><region name="Connecticut"><name sortKey="Yu, Pengchun" sort="Yu, Pengchun" uniqKey="Yu P" first="Pengchun" last="Yu">Pengchun Yu</name></region><name sortKey="Simons, Michael" sort="Simons, Michael" uniqKey="Simons M" first="Michael" last="Simons">Michael Simons</name><name sortKey="Tung, Joe K" sort="Tung, Joe K" uniqKey="Tung J" first="Joe K" last="Tung">Joe K. 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