Adrenomedullin Haploinsufficiency Predisposes to Secondary Lymphedema
Identifieur interne : 003904 ( Main/Exploration ); précédent : 003903; suivant : 003905Adrenomedullin Haploinsufficiency Predisposes to Secondary Lymphedema
Auteurs : Leonid L. Nikitenko [Royaume-Uni] ; Tatsuo Shimosawa [Japon] ; Stephen Henderson [Royaume-Uni] ; Taija M Kinen [Royaume-Uni] ; Hiromi Shimosawa [Japon] ; Uzma Qureshi [Royaume-Uni] ; R Barbara Pedley [Royaume-Uni] ; Margaret C P. Rees [Royaume-Uni] ; Toshiro Fujita [Japon] ; Chris Boshoff [Royaume-Uni]Source :
- The Journal of Investigative Dermatology [ 0022-202X ] ; 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
Url:
DOI: 10.1038/jid.2013.47
PubMed: 23364478
PubMed Central: 3682392
Affiliations:
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Le document en format XML
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<series><title level="j">The Journal of Investigative Dermatology</title>
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<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>
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<front><div type="abstract" xml:lang="en"><p>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 <italic>Adm</italic>
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 <italic>Adm</italic>
gene-knockin stop mutation, which selectively abrogated AM, but preserved PAMP, expression (<italic>Adm</italic>
<sup><italic>AM+/Δ</italic>
</sup>
animals). After hind limb skin incision, <italic>Adm</italic>
messenger RNA expression was upregulated in wounded tissue of both <italic>Adm</italic>
<sup><italic>AM+/+</italic>
</sup>
and <italic>Adm</italic>
<sup><italic>AM+/Δ</italic>
</sup>
mice. However, only <italic>Adm</italic>
<sup><italic>AM+/Δ</italic>
</sup>
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 <italic>Adm</italic>
<sup><italic>AM+/Δ</italic>
</sup>
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 <italic>in vivo</italic>
evidence of an underlying germ-line genetic predisposition to developing this disorder.</p>
</div>
</front>
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