Adrenomedullin haploinsufficiency predisposes to secondary lymphedema.
Identifieur interne : 001C64 ( PubMed/Checkpoint ); précédent : 001C63; suivant : 001C65Adrenomedullin haploinsufficiency predisposes to secondary lymphedema.
Auteurs : Leonid L. Nikitenko [Royaume-Uni] ; Tatsuo Shimosawa ; Stephen Henderson ; Taija M Kinen ; Hiromi Shimosawa ; Uzma Qureshi ; R Barbara Pedley ; Margaret C P. Rees ; Toshiro Fujita ; Chris BoshoffSource :
- The Journal of investigative dermatology [ 1523-1747 ] ; 2013.
Descripteurs français
- KwdFr :
- Adrénomédulline (génétique), Animaux, Cellules cultivées, Endothélium lymphatique (métabolisme), Endothélium vasculaire (métabolisme), Facteurs de risque, Haploinsuffisance (génétique), Humains, Hétérozygote, Lymphoedème (génétique), Mutation (génétique), Phénotype, Protéine apparentée au récepteur de la calcitonine (métabolisme), Prédisposition génétique à une maladie (génétique), Souches mutantes de souris, Souris, Souris de lignée C57BL, Techniques de knock-in de gènes.
- MESH :
- génétique : Adrénomédulline, Haploinsuffisance, Lymphoedème, Mutation, Prédisposition génétique à une maladie.
- métabolisme : Endothélium lymphatique, Endothélium vasculaire, Protéine apparentée au récepteur de la calcitonine.
- Animaux, Cellules cultivées, Facteurs de risque, Humains, Hétérozygote, Phénotype, Souches mutantes de souris, Souris, Souris de lignée C57BL, Techniques de knock-in de gènes.
English descriptors
- KwdEn :
- Adrenomedullin (genetics), Animals, Calcitonin Receptor-Like Protein (metabolism), Cells, Cultured, Endothelium, Lymphatic (metabolism), Endothelium, Vascular (metabolism), Gene Knock-In Techniques, Genetic Predisposition to Disease (genetics), Haploinsufficiency (genetics), Heterozygote, Humans, Lymphedema (genetics), Mice, Mice, Inbred C57BL, Mice, Mutant Strains, Mutation (genetics), Phenotype, Risk Factors.
- MESH :
- chemical , genetics : Adrenomedullin.
- chemical , metabolism : Calcitonin Receptor-Like Protein.
- genetics : Genetic Predisposition to Disease, Haploinsufficiency, Lymphedema, Mutation.
- metabolism : Endothelium, Lymphatic, Endothelium, Vascular.
- Animals, Cells, Cultured, Gene Knock-In Techniques, Heterozygote, Humans, Mice, Mice, Inbred C57BL, Mice, Mutant Strains, Phenotype, Risk Factors.
Abstract
Secondary lymphedema is a debilitating condition, and genetic factors predisposing to its development remain largely unknown. Adrenomedullin (AM) is peptide encoded, together with proadrenomedullin N-terminal peptide (PAMP), by the Adm gene (adrenomedullin gene). AM and its putative receptor calcitonin receptor-like receptor (CLR) are implicated in angiogenesis and lymphangiogenesis during embryogenesis and wound healing, suggesting their possible involvement in secondary lymphedema. To investigate whether AM deficiency predisposes to secondary lymphedema, we used heterozygous adult mice with Adm gene-knockin stop mutation, which selectively abrogated AM, but preserved PAMP, expression (Adm(AM+/Δ) animals). After hind limb skin incision, Adm messenger RNA expression was upregulated in wounded tissue of both Adm(AM+/+) and Adm(AM+/Δ) mice. However, only Adm(AM+/Δ) animals developed limb swelling and histopathological lymphedematous changes, including epidermal thickening, elevated collagen fiber density, and increased microvessel diameter. Secondary lymphedema was prevented when circulating AM levels in Adm(AM+/Δ) mice were restored by systemic peptide delivery. In human skin, CLR was expressed in tissue components affected by lymphedema, including epidermis, lymphatics, and blood vessels. Our study identified a previously unrecognized role for endogenous AM as a key factor in secondary lymphedema pathogenesis and provided experimental in vivo evidence of an underlying germ-line genetic predisposition to developing this disorder.
DOI: 10.1038/jid.2013.47
PubMed: 23364478
Affiliations:
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pubmed:23364478Le document en format XML
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Rees</name></author><author><name sortKey="Fujita, Toshiro" sort="Fujita, Toshiro" uniqKey="Fujita T" first="Toshiro" last="Fujita">Toshiro Fujita</name></author><author><name sortKey="Boshoff, Chris" sort="Boshoff, Chris" uniqKey="Boshoff C" first="Chris" last="Boshoff">Chris Boshoff</name></author></analytic><series><title level="j">The Journal of investigative dermatology</title><idno type="eISSN">1523-1747</idno><imprint><date when="2013" type="published">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adrenomedullin (genetics)</term><term>Animals</term><term>Calcitonin Receptor-Like Protein (metabolism)</term><term>Cells, Cultured</term><term>Endothelium, Lymphatic (metabolism)</term><term>Endothelium, Vascular (metabolism)</term><term>Gene Knock-In Techniques</term><term>Genetic Predisposition to Disease (genetics)</term><term>Haploinsufficiency (genetics)</term><term>Heterozygote</term><term>Humans</term><term>Lymphedema (genetics)</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Mutant Strains</term><term>Mutation (genetics)</term><term>Phenotype</term><term>Risk Factors</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adrénomédulline (génétique)</term><term>Animaux</term><term>Cellules cultivées</term><term>Endothélium lymphatique (métabolisme)</term><term>Endothélium vasculaire (métabolisme)</term><term>Facteurs de risque</term><term>Haploinsuffisance (génétique)</term><term>Humains</term><term>Hétérozygote</term><term>Lymphoedème (génétique)</term><term>Mutation (génétique)</term><term>Phénotype</term><term>Protéine apparentée au récepteur de la calcitonine (métabolisme)</term><term>Prédisposition génétique à une maladie (génétique)</term><term>Souches mutantes de souris</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Techniques de knock-in de gènes</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Adrenomedullin</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Calcitonin Receptor-Like Protein</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Genetic Predisposition to Disease</term><term>Haploinsufficiency</term><term>Lymphedema</term><term>Mutation</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Adrénomédulline</term><term>Haploinsuffisance</term><term>Lymphoedème</term><term>Mutation</term><term>Prédisposition génétique à une maladie</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Endothelium, Lymphatic</term><term>Endothelium, Vascular</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Endothélium lymphatique</term><term>Endothélium vasculaire</term><term>Protéine apparentée au récepteur de la calcitonine</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cells, Cultured</term><term>Gene Knock-In Techniques</term><term>Heterozygote</term><term>Humans</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Mutant Strains</term><term>Phenotype</term><term>Risk Factors</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules cultivées</term><term>Facteurs de risque</term><term>Humains</term><term>Hétérozygote</term><term>Phénotype</term><term>Souches mutantes de souris</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Techniques de knock-in de gènes</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Secondary lymphedema is a debilitating condition, and genetic factors predisposing to its development remain largely unknown. Adrenomedullin (AM) is peptide encoded, together with proadrenomedullin N-terminal peptide (PAMP), by the Adm gene (adrenomedullin gene). AM and its putative receptor calcitonin receptor-like receptor (CLR) are implicated in angiogenesis and lymphangiogenesis during embryogenesis and wound healing, suggesting their possible involvement in secondary lymphedema. To investigate whether AM deficiency predisposes to secondary lymphedema, we used heterozygous adult mice with Adm gene-knockin stop mutation, which selectively abrogated AM, but preserved PAMP, expression (Adm(AM+/Δ) animals). After hind limb skin incision, Adm messenger RNA expression was upregulated in wounded tissue of both Adm(AM+/+) and Adm(AM+/Δ) mice. However, only Adm(AM+/Δ) animals developed limb swelling and histopathological lymphedematous changes, including epidermal thickening, elevated collagen fiber density, and increased microvessel diameter. Secondary lymphedema was prevented when circulating AM levels in Adm(AM+/Δ) mice were restored by systemic peptide delivery. In human skin, CLR was expressed in tissue components affected by lymphedema, including epidermis, lymphatics, and blood vessels. Our study identified a previously unrecognized role for endogenous AM as a key factor in secondary lymphedema pathogenesis and provided experimental in vivo evidence of an underlying germ-line genetic predisposition to developing this disorder.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23364478</PMID><DateCreated><Year>2013</Year><Month>06</Month><Day>13</Day></DateCreated><DateCompleted><Year>2013</Year><Month>09</Month><Day>04</Day></DateCompleted><DateRevised><Year>2017</Year><Month>09</Month><Day>02</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1523-1747</ISSN><JournalIssue CitedMedium="Internet"><Volume>133</Volume><Issue>7</Issue><PubDate><Year>2013</Year><Month>Jul</Month></PubDate></JournalIssue><Title>The Journal of investigative dermatology</Title><ISOAbbreviation>J. Invest. Dermatol.</ISOAbbreviation></Journal><ArticleTitle>Adrenomedullin haploinsufficiency predisposes to secondary lymphedema.</ArticleTitle><Pagination><MedlinePgn>1768-76</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/jid.2013.47</ELocationID><Abstract><AbstractText>Secondary lymphedema is a debilitating condition, and genetic factors predisposing to its development remain largely unknown. Adrenomedullin (AM) is peptide encoded, together with proadrenomedullin N-terminal peptide (PAMP), by the Adm gene (adrenomedullin gene). AM and its putative receptor calcitonin receptor-like receptor (CLR) are implicated in angiogenesis and lymphangiogenesis during embryogenesis and wound healing, suggesting their possible involvement in secondary lymphedema. To investigate whether AM deficiency predisposes to secondary lymphedema, we used heterozygous adult mice with Adm gene-knockin stop mutation, which selectively abrogated AM, but preserved PAMP, expression (Adm(AM+/Δ) animals). After hind limb skin incision, Adm messenger RNA expression was upregulated in wounded tissue of both Adm(AM+/+) and Adm(AM+/Δ) mice. However, only Adm(AM+/Δ) animals developed limb swelling and histopathological lymphedematous changes, including epidermal thickening, elevated collagen fiber density, and increased microvessel diameter. Secondary lymphedema was prevented when circulating AM levels in Adm(AM+/Δ) mice were restored by systemic peptide delivery. In human skin, CLR was expressed in tissue components affected by lymphedema, including epidermis, lymphatics, and blood vessels. Our study identified a previously unrecognized role for endogenous AM as a key factor in secondary lymphedema pathogenesis and provided experimental in vivo evidence of an underlying germ-line genetic predisposition to developing this disorder.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Nikitenko</LastName><ForeName>Leonid L</ForeName><Initials>LL</Initials><AffiliationInfo><Affiliation>Cancer Research UK Viral Oncology Group, UCL Cancer Institute, University College London, London, UK. l.nikitenko@ucl.ac.uk</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shimosawa</LastName><ForeName>Tatsuo</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Henderson</LastName><ForeName>Stephen</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Mäkinen</LastName><ForeName>Taija</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Shimosawa</LastName><ForeName>Hiromi</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Qureshi</LastName><ForeName>Uzma</ForeName><Initials>U</Initials></Author><Author ValidYN="Y"><LastName>Pedley</LastName><ForeName>R Barbara</ForeName><Initials>RB</Initials></Author><Author ValidYN="Y"><LastName>Rees</LastName><ForeName>Margaret C P</ForeName><Initials>MC</Initials></Author><Author ValidYN="Y"><LastName>Fujita</LastName><ForeName>Toshiro</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Boshoff</LastName><ForeName>Chris</ForeName><Initials>C</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>MRC_G1001497</GrantID><Agency>Medical Research Council</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>C575/A13100</GrantID><Agency>Cancer Research UK</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>C575/A6125</GrantID><Agency>Cancer Research UK</Agency><Country>United Kingdom</Country></Grant><Grant><Agency>Wellcome Trust</Agency><Country>United Kingdom</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2013</Year><Month>01</Month><Day>30</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Invest Dermatol</MedlineTA><NlmUniqueID>0426720</NlmUniqueID><ISSNLinking>0022-202X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D058286">Calcitonin Receptor-Like Protein</NameOfSubstance></Chemical><Chemical><RegistryNumber>148498-78-6</RegistryNumber><NameOfSubstance UI="D053607">Adrenomedullin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections 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Invest. 2011 Aug;121(8):2984-92</RefSource><PMID Version="1">21765212</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Genet. 2011 Oct;43(10):929-31</RefSource><PMID Version="1">21892158</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nature. 2011 Oct 6;478(7367):103-9</RefSource><PMID Version="1">21909115</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Scanning. 2011 Nov-Dec;33(6):463-7</RefSource><PMID Version="1">21796645</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2001 Jan 16;98(2):615-9</RefSource><PMID Version="1">11149956</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D053607" MajorTopicYN="N">Adrenomedullin</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D058286" MajorTopicYN="N">Calcitonin Receptor-Like Protein</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004729" MajorTopicYN="N">Endothelium, Lymphatic</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004730" MajorTopicYN="N">Endothelium, Vascular</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D055879" MajorTopicYN="Y">Gene Knock-In Techniques</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020022" MajorTopicYN="N">Genetic Predisposition to Disease</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D057895" MajorTopicYN="N">Haploinsufficiency</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006579" MajorTopicYN="N">Heterozygote</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008209" MajorTopicYN="N">Lymphedema</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008817" MajorTopicYN="N">Mice, Mutant Strains</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009154" MajorTopicYN="N">Mutation</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010641" MajorTopicYN="N">Phenotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012307" MajorTopicYN="N">Risk Factors</DescriptorName></MeshHeading></MeshHeadingList><OtherID Source="NLM">PMC3682392</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2013</Year><Month>2</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2013</Year><Month>2</Month><Day>1</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2013</Year><Month>9</Month><Day>5</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">23364478</ArticleId><ArticleId IdType="pii">S0022-202X(15)36336-3</ArticleId><ArticleId IdType="doi">10.1038/jid.2013.47</ArticleId><ArticleId IdType="pmc">PMC3682392</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Royaume-Uni</li></country><region><li>Angleterre</li><li>Grand Londres</li></region><settlement><li>Londres</li></settlement><orgName><li>University College de Londres</li></orgName></list><tree><noCountry><name sortKey="Boshoff, Chris" sort="Boshoff, Chris" uniqKey="Boshoff C" first="Chris" last="Boshoff">Chris Boshoff</name><name sortKey="Fujita, Toshiro" sort="Fujita, Toshiro" uniqKey="Fujita T" first="Toshiro" last="Fujita">Toshiro Fujita</name><name sortKey="Henderson, Stephen" sort="Henderson, Stephen" uniqKey="Henderson S" first="Stephen" last="Henderson">Stephen Henderson</name><name sortKey="M Kinen, Taija" sort="M Kinen, Taija" uniqKey="M Kinen T" first="Taija" last="M Kinen">Taija M Kinen</name><name sortKey="Pedley, R Barbara" sort="Pedley, R Barbara" uniqKey="Pedley R" first="R Barbara" last="Pedley">R Barbara Pedley</name><name sortKey="Qureshi, Uzma" sort="Qureshi, Uzma" uniqKey="Qureshi U" first="Uzma" last="Qureshi">Uzma Qureshi</name><name sortKey="Rees, Margaret C P" sort="Rees, Margaret C P" uniqKey="Rees M" first="Margaret C P" last="Rees">Margaret C P. Rees</name><name sortKey="Shimosawa, Hiromi" sort="Shimosawa, Hiromi" uniqKey="Shimosawa H" first="Hiromi" last="Shimosawa">Hiromi Shimosawa</name><name sortKey="Shimosawa, Tatsuo" sort="Shimosawa, Tatsuo" uniqKey="Shimosawa T" first="Tatsuo" last="Shimosawa">Tatsuo Shimosawa</name></noCountry><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Nikitenko, Leonid L" sort="Nikitenko, Leonid L" uniqKey="Nikitenko L" first="Leonid L" last="Nikitenko">Leonid L. Nikitenko</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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