G protein-coupled receptors as potential drug targets for lymphangiogenesis and lymphatic vascular diseases.
Identifieur interne : 002F52 ( PubMed/Curation ); précédent : 002F51; suivant : 002F53G protein-coupled receptors as potential drug targets for lymphangiogenesis and lymphatic vascular diseases.
Auteurs : William P. Dunworth [États-Unis] ; Kathleen M. CaronSource :
- Arteriosclerosis, thrombosis, and vascular biology [ 1524-4636 ] ; 2009.
Descripteurs français
- KwdFr :
- Animaux, Endothélium lymphatique (), Endothélium lymphatique (physiologie), Humains, Lymphangiogenèse (), Lymphangiogenèse (physiologie), Lymphoedème (physiopathologie), Lymphoedème (traitement médicamenteux), Protéine apparentée au récepteur de la calcitonine, Récepteurs aux lysophospholipides (physiologie), Récepteurs couplés aux protéines G (), Récepteurs couplés aux protéines G (physiologie), Récepteurs à la calcitonine (physiologie), Souris, Souris knockout.
- MESH :
- physiologie : Endothélium lymphatique, Lymphangiogenèse, Récepteurs aux lysophospholipides, Récepteurs couplés aux protéines G, Récepteurs à la calcitonine.
- physiopathologie : Lymphoedème.
- traitement médicamenteux : Lymphoedème.
- Animaux, Endothélium lymphatique, Humains, Lymphangiogenèse, Protéine apparentée au récepteur de la calcitonine, Récepteurs couplés aux protéines G, Souris, Souris knockout.
English descriptors
- KwdEn :
- Animals, Calcitonin Receptor-Like Protein, Endothelium, Lymphatic (drug effects), Endothelium, Lymphatic (physiology), Humans, Lymphangiogenesis (drug effects), Lymphangiogenesis (physiology), Lymphedema (drug therapy), Lymphedema (physiopathology), Mice, Mice, Knockout, Receptors, Calcitonin (physiology), Receptors, G-Protein-Coupled (drug effects), Receptors, G-Protein-Coupled (physiology), Receptors, Lysophospholipid (physiology).
- MESH :
- chemical , drug effects : Receptors, G-Protein-Coupled.
- chemical , physiology : Receptors, Calcitonin, Receptors, G-Protein-Coupled, Receptors, Lysophospholipid.
- chemical : Calcitonin Receptor-Like Protein.
- drug effects : Endothelium, Lymphatic, Lymphangiogenesis.
- drug therapy : Lymphedema.
- physiology : Endothelium, Lymphatic, Lymphangiogenesis.
- physiopathology : Lymphedema.
- Animals, Humans, Mice, Mice, Knockout.
Abstract
G protein-coupled receptors (GPCRs) are widely expressed cell surface receptors that have been successfully exploited for the treatment of a variety of human diseases. Recent studies in genetically engineered mouse models have led to the identification of several GPCRs important for lymphatic vascular development and function. The adrenomedullin receptor, which consists of an oligomer between calcitonin receptor-like receptor and receptor activity modifying protein 2, is required for normal lymphatic vascular development and regulates lymphatic capillary permeability in mice. Numerous studies also suggest that lysophospholipid receptors are involved in the development of lymphatic vessels and lymphatic endothelial cell permeability. Given our current lack of pharmacological targets for the treatment of lymphatic vascular diseases like lymphedema, the continued identification and study of GPCRs in lymphatic endothelial cells may eventually lead to major breakthroughs and new pharmacological strategies for the treatment of lymphedema.
DOI: 10.1161/ATVBAHA.109.185066
PubMed: 19265032
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">G protein-coupled receptors as potential drug targets for lymphangiogenesis and lymphatic vascular diseases.</title><author><name sortKey="Dunworth, William P" sort="Dunworth, William P" uniqKey="Dunworth W" first="William P" last="Dunworth">William P. Dunworth</name><affiliation wicri:level="1"><nlm:affiliation>Department of Cell and Molecular Physiology, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Cell and Molecular Physiology, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599</wicri:regionArea></affiliation></author><author><name sortKey="Caron, Kathleen M" sort="Caron, Kathleen M" uniqKey="Caron K" first="Kathleen M" last="Caron">Kathleen M. Caron</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2009">2009</date><idno type="RBID">pubmed:19265032</idno><idno type="pmid">19265032</idno><idno type="doi">10.1161/ATVBAHA.109.185066</idno><idno type="wicri:Area/PubMed/Corpus">002F52</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">002F52</idno><idno type="wicri:Area/PubMed/Curation">002F52</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">002F52</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">G protein-coupled receptors as potential drug targets for lymphangiogenesis and lymphatic vascular diseases.</title><author><name sortKey="Dunworth, William P" sort="Dunworth, William P" uniqKey="Dunworth W" first="William P" last="Dunworth">William P. Dunworth</name><affiliation wicri:level="1"><nlm:affiliation>Department of Cell and Molecular Physiology, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Cell and Molecular Physiology, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599</wicri:regionArea></affiliation></author><author><name sortKey="Caron, Kathleen M" sort="Caron, Kathleen M" uniqKey="Caron K" first="Kathleen M" last="Caron">Kathleen M. Caron</name></author></analytic><series><title level="j">Arteriosclerosis, thrombosis, and vascular biology</title><idno type="eISSN">1524-4636</idno><imprint><date when="2009" type="published">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Calcitonin Receptor-Like Protein</term><term>Endothelium, Lymphatic (drug effects)</term><term>Endothelium, Lymphatic (physiology)</term><term>Humans</term><term>Lymphangiogenesis (drug effects)</term><term>Lymphangiogenesis (physiology)</term><term>Lymphedema (drug therapy)</term><term>Lymphedema (physiopathology)</term><term>Mice</term><term>Mice, Knockout</term><term>Receptors, Calcitonin (physiology)</term><term>Receptors, G-Protein-Coupled (drug effects)</term><term>Receptors, G-Protein-Coupled (physiology)</term><term>Receptors, Lysophospholipid (physiology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Endothélium lymphatique ()</term><term>Endothélium lymphatique (physiologie)</term><term>Humains</term><term>Lymphangiogenèse ()</term><term>Lymphangiogenèse (physiologie)</term><term>Lymphoedème (physiopathologie)</term><term>Lymphoedème (traitement médicamenteux)</term><term>Protéine apparentée au récepteur de la calcitonine</term><term>Récepteurs aux lysophospholipides (physiologie)</term><term>Récepteurs couplés aux protéines G ()</term><term>Récepteurs couplés aux protéines G (physiologie)</term><term>Récepteurs à la calcitonine (physiologie)</term><term>Souris</term><term>Souris knockout</term></keywords><keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>Receptors, G-Protein-Coupled</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Receptors, Calcitonin</term><term>Receptors, G-Protein-Coupled</term><term>Receptors, Lysophospholipid</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Calcitonin Receptor-Like Protein</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Endothelium, Lymphatic</term><term>Lymphangiogenesis</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Lymphedema</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Endothélium lymphatique</term><term>Lymphangiogenèse</term><term>Récepteurs aux lysophospholipides</term><term>Récepteurs couplés aux protéines G</term><term>Récepteurs à la calcitonine</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Endothelium, Lymphatic</term><term>Lymphangiogenesis</term></keywords><keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Lymphoedème</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Lymphedema</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Lymphoedème</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term><term>Mice</term><term>Mice, Knockout</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Endothélium lymphatique</term><term>Humains</term><term>Lymphangiogenèse</term><term>Protéine apparentée au récepteur de la calcitonine</term><term>Récepteurs couplés aux protéines G</term><term>Souris</term><term>Souris knockout</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">G protein-coupled receptors (GPCRs) are widely expressed cell surface receptors that have been successfully exploited for the treatment of a variety of human diseases. Recent studies in genetically engineered mouse models have led to the identification of several GPCRs important for lymphatic vascular development and function. The adrenomedullin receptor, which consists of an oligomer between calcitonin receptor-like receptor and receptor activity modifying protein 2, is required for normal lymphatic vascular development and regulates lymphatic capillary permeability in mice. Numerous studies also suggest that lysophospholipid receptors are involved in the development of lymphatic vessels and lymphatic endothelial cell permeability. Given our current lack of pharmacological targets for the treatment of lymphatic vascular diseases like lymphedema, the continued identification and study of GPCRs in lymphatic endothelial cells may eventually lead to major breakthroughs and new pharmacological strategies for the treatment of lymphedema.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">19265032</PMID><DateCreated><Year>2009</Year><Month>04</Month><Day>16</Day></DateCreated><DateCompleted><Year>2009</Year><Month>05</Month><Day>13</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>22</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1524-4636</ISSN><JournalIssue CitedMedium="Internet"><Volume>29</Volume><Issue>5</Issue><PubDate><Year>2009</Year><Month>May</Month></PubDate></JournalIssue><Title>Arteriosclerosis, thrombosis, and vascular biology</Title><ISOAbbreviation>Arterioscler. Thromb. Vasc. Biol.</ISOAbbreviation></Journal><ArticleTitle>G protein-coupled receptors as potential drug targets for lymphangiogenesis and lymphatic vascular diseases.</ArticleTitle><Pagination><MedlinePgn>650-6</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1161/ATVBAHA.109.185066</ELocationID><Abstract><AbstractText>G protein-coupled receptors (GPCRs) are widely expressed cell surface receptors that have been successfully exploited for the treatment of a variety of human diseases. Recent studies in genetically engineered mouse models have led to the identification of several GPCRs important for lymphatic vascular development and function. The adrenomedullin receptor, which consists of an oligomer between calcitonin receptor-like receptor and receptor activity modifying protein 2, is required for normal lymphatic vascular development and regulates lymphatic capillary permeability in mice. Numerous studies also suggest that lysophospholipid receptors are involved in the development of lymphatic vessels and lymphatic endothelial cell permeability. Given our current lack of pharmacological targets for the treatment of lymphatic vascular diseases like lymphedema, the continued identification and study of GPCRs in lymphatic endothelial cells may eventually lead to major breakthroughs and new pharmacological strategies for the treatment of lymphedema.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Dunworth</LastName><ForeName>William P</ForeName><Initials>WP</Initials><AffiliationInfo><Affiliation>Department of Cell and Molecular Physiology, The University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Caron</LastName><ForeName>Kathleen M</ForeName><Initials>KM</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 HL091973</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL091973-01</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HL091973-02</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>HL091973</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><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2009</Year><Month>03</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Arterioscler Thromb Vasc 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MajorTopicYN="N">Calcitonin Receptor-Like Protein</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004729" MajorTopicYN="N">Endothelium, Lymphatic</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D042583" MajorTopicYN="N">Lymphangiogenesis</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008209" MajorTopicYN="N">Lymphedema</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018003" MajorTopicYN="N">Receptors, Calcitonin</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D043562" MajorTopicYN="N">Receptors, G-Protein-Coupled</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D049312" MajorTopicYN="N">Receptors, Lysophospholipid</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>89</NumberOfReferences><OtherID Source="NLM">NIHMS126167</OtherID><OtherID Source="NLM">PMC2761011</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2009</Year><Month>3</Month><Day>7</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2009</Year><Month>3</Month><Day>7</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2009</Year><Month>5</Month><Day>14</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">19265032</ArticleId><ArticleId IdType="pii">ATVBAHA.109.185066</ArticleId><ArticleId IdType="doi">10.1161/ATVBAHA.109.185066</ArticleId><ArticleId IdType="pmc">PMC2761011</ArticleId><ArticleId IdType="mid">NIHMS126167</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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