Interleukin-8 reduces post-surgical lymphedema formation by promoting lymphatic vessel regeneration.
Identifieur interne : 001A86 ( PubMed/Checkpoint ); précédent : 001A85; suivant : 001A87Interleukin-8 reduces post-surgical lymphedema formation by promoting lymphatic vessel regeneration.
Auteurs : Inho Choi [États-Unis] ; Yong Suk Lee ; Hee Kyoung Chung ; Dongwon Choi ; Tatiana Ecoiffier ; Ha Neul Lee ; Kyu Eui Kim ; Sunju Lee ; Eun Kyung Park ; Yong Sun Maeng ; Nam Yun Kim ; Robert D. Ladner ; Nicos A. Petasis ; Chester J. Koh ; Lu Chen ; Heinz-Josef Lenz ; Young-Kwon HongSource :
- Angiogenesis [ 1573-7209 ] ; 2013.
Descripteurs français
- KwdFr :
- Animaux, Cellules cultivées, Cellules endothéliales (), Cellules endothéliales (métabolisme), Complications postopératoires (anatomopathologie), Complications postopératoires (physiopathologie), Complications postopératoires (traitement médicamenteux), Complications postopératoires (étiologie), Développement embryonnaire (), Facteur de nécrose tumorale alpha (pharmacologie), Humains, Inhibiteur p57 de kinase cycline-dépendante (métabolisme), Interleukine-8 (métabolisme), Interleukine-8 (pharmacologie), Interleukine-8 (usage thérapeutique), Lymphangiogenèse (), Lymphoedème (anatomopathologie), Lymphoedème (physiopathologie), Lymphoedème (traitement médicamenteux), Lymphoedème (étiologie), Microenvironnement tumoral (), Néovascularisation physiologique (), Prolifération cellulaire (), Protéines suppresseurs de tumeurs (métabolisme), Protéines à homéodomaine (métabolisme), Récepteurs à l'interleukine-8 (métabolisme), Récepteurs à l'interleukine-8A (métabolisme), Récepteurs à l'interleukine-8B (métabolisme), Régulation négative (), Régénération (), Souris, Souris transgéniques, Trétinoïne (pharmacologie), Vaisseaux lymphatiques (), Vaisseaux lymphatiques (anatomopathologie), Vaisseaux lymphatiques (physiopathologie).
- MESH :
- anatomopathologie : Complications postopératoires, Lymphoedème, Vaisseaux lymphatiques.
- métabolisme : Cellules endothéliales, Inhibiteur p57 de kinase cycline-dépendante, Interleukine-8, Protéines suppresseurs de tumeurs, Protéines à homéodomaine, Récepteurs à l'interleukine-8, Récepteurs à l'interleukine-8A, Récepteurs à l'interleukine-8B.
- pharmacologie : Facteur de nécrose tumorale alpha, Interleukine-8, Trétinoïne.
- physiopathologie : Complications postopératoires, Lymphoedème, Vaisseaux lymphatiques.
- traitement médicamenteux : Complications postopératoires, Lymphoedème.
- usage thérapeutique : Interleukine-8.
- étiologie : Complications postopératoires, Lymphoedème.
- Animaux, Cellules cultivées, Cellules endothéliales, Développement embryonnaire, Humains, Lymphangiogenèse, Microenvironnement tumoral, Néovascularisation physiologique, Prolifération cellulaire, Régulation négative, Régénération, Souris, Souris transgéniques, Vaisseaux lymphatiques.
English descriptors
- KwdEn :
- Animals, Cell Proliferation (drug effects), Cells, Cultured, Cyclin-Dependent Kinase Inhibitor p57 (metabolism), Down-Regulation (drug effects), Embryonic Development (drug effects), Endothelial Cells (drug effects), Endothelial Cells (metabolism), Homeodomain Proteins (metabolism), Humans, Interleukin-8 (metabolism), Interleukin-8 (pharmacology), Interleukin-8 (therapeutic use), Lymphangiogenesis (drug effects), Lymphatic Vessels (drug effects), Lymphatic Vessels (pathology), Lymphatic Vessels (physiopathology), Lymphedema (drug therapy), Lymphedema (etiology), Lymphedema (pathology), Lymphedema (physiopathology), Mice, Mice, Transgenic, Neovascularization, Physiologic (drug effects), Postoperative Complications (drug therapy), Postoperative Complications (etiology), Postoperative Complications (pathology), Postoperative Complications (physiopathology), Receptors, Interleukin-8 (metabolism), Receptors, Interleukin-8A (metabolism), Receptors, Interleukin-8B (metabolism), Regeneration (drug effects), Tretinoin (pharmacology), Tumor Microenvironment (drug effects), Tumor Necrosis Factor-alpha (pharmacology), Tumor Suppressor Proteins (metabolism).
- MESH :
- chemical , metabolism : Cyclin-Dependent Kinase Inhibitor p57, Homeodomain Proteins, Interleukin-8, Receptors, Interleukin-8, Receptors, Interleukin-8A, Receptors, Interleukin-8B, Tumor Suppressor Proteins.
- drug effects : Cell Proliferation, Down-Regulation, Embryonic Development, Endothelial Cells, Lymphangiogenesis, Lymphatic Vessels, Neovascularization, Physiologic, Regeneration, Tumor Microenvironment.
- drug therapy : Lymphedema, Postoperative Complications.
- etiology : Lymphedema, Postoperative Complications.
- metabolism : Endothelial Cells.
- pathology : Lymphatic Vessels, Lymphedema, Postoperative Complications.
- chemical , pharmacology : Interleukin-8, Tretinoin, Tumor Necrosis Factor-alpha.
- physiopathology : Lymphatic Vessels, Lymphedema, Postoperative Complications.
- chemical , therapeutic use : Interleukin-8.
- Animals, Cells, Cultured, Humans, Mice, Mice, Transgenic.
Abstract
Lymphedema is mainly caused by lymphatic obstruction and manifested as tissue swelling, often in the arms and legs. Lymphedema is one of the most common post-surgical complications in breast cancer patients and presents a painful and disfiguring chronic illness that has few treatment options. Here, we evaluated the therapeutic potential of interleukin (IL)-8 in lymphatic regeneration independent of its pro-inflammatory activity. We found that IL-8 promoted proliferation, tube formation, and migration of lymphatic endothelial cells (LECs) without activating the VEGF signaling. Additionally, IL-8 suppressed the major cell cycle inhibitor CDKN1C/p57(KIP2) by downregulating its positive regulator PROX1, which is known as the master regulator of LEC-differentiation. Animal-based studies such as matrigel plug and cornea micropocket assays demonstrated potent efficacy of IL-8 in activating lymphangiogenesis in vivo. Moreover, we have generated a novel transgenic mouse model (K14-hIL8) that expresses human IL-8 in the skin and then crossed with lymphatic-specific fluorescent (Prox1-GFP) mouse. The resulting double transgenic mice showed that a stable expression of IL-8 could promote embryonic lymphangiogenesis. Moreover, an immunodeficient IL-8-expressing mouse line that was established by crossing K14-hIL8 mice with athymic nude mice displayed an enhanced tumor-associated lymphangiogenesis. Finally, when experimental lymphedema was introduced, K14-hIL8 mice showed an improved amelioration of lymphedema with an increased lymphatic regeneration. Together, we report that IL-8 can activate lymphangiogenesis in vitro and in vivo with a therapeutic efficacy in post-surgical lymphedema.
DOI: 10.1007/s10456-012-9297-6
PubMed: 22945845
Affiliations:
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pubmed:22945845Le document en format XML
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<series><title level="j">Angiogenesis</title>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term>
<term>Cell Proliferation (drug effects)</term>
<term>Cells, Cultured</term>
<term>Cyclin-Dependent Kinase Inhibitor p57 (metabolism)</term>
<term>Down-Regulation (drug effects)</term>
<term>Embryonic Development (drug effects)</term>
<term>Endothelial Cells (drug effects)</term>
<term>Endothelial Cells (metabolism)</term>
<term>Homeodomain Proteins (metabolism)</term>
<term>Humans</term>
<term>Interleukin-8 (metabolism)</term>
<term>Interleukin-8 (pharmacology)</term>
<term>Interleukin-8 (therapeutic use)</term>
<term>Lymphangiogenesis (drug effects)</term>
<term>Lymphatic Vessels (drug effects)</term>
<term>Lymphatic Vessels (pathology)</term>
<term>Lymphatic Vessels (physiopathology)</term>
<term>Lymphedema (drug therapy)</term>
<term>Lymphedema (etiology)</term>
<term>Lymphedema (pathology)</term>
<term>Lymphedema (physiopathology)</term>
<term>Mice</term>
<term>Mice, Transgenic</term>
<term>Neovascularization, Physiologic (drug effects)</term>
<term>Postoperative Complications (drug therapy)</term>
<term>Postoperative Complications (etiology)</term>
<term>Postoperative Complications (pathology)</term>
<term>Postoperative Complications (physiopathology)</term>
<term>Receptors, Interleukin-8 (metabolism)</term>
<term>Receptors, Interleukin-8A (metabolism)</term>
<term>Receptors, Interleukin-8B (metabolism)</term>
<term>Regeneration (drug effects)</term>
<term>Tretinoin (pharmacology)</term>
<term>Tumor Microenvironment (drug effects)</term>
<term>Tumor Necrosis Factor-alpha (pharmacology)</term>
<term>Tumor Suppressor Proteins (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Cellules cultivées</term>
<term>Cellules endothéliales ()</term>
<term>Cellules endothéliales (métabolisme)</term>
<term>Complications postopératoires (anatomopathologie)</term>
<term>Complications postopératoires (physiopathologie)</term>
<term>Complications postopératoires (traitement médicamenteux)</term>
<term>Complications postopératoires (étiologie)</term>
<term>Développement embryonnaire ()</term>
<term>Facteur de nécrose tumorale alpha (pharmacologie)</term>
<term>Humains</term>
<term>Inhibiteur p57 de kinase cycline-dépendante (métabolisme)</term>
<term>Interleukine-8 (métabolisme)</term>
<term>Interleukine-8 (pharmacologie)</term>
<term>Interleukine-8 (usage thérapeutique)</term>
<term>Lymphangiogenèse ()</term>
<term>Lymphoedème (anatomopathologie)</term>
<term>Lymphoedème (physiopathologie)</term>
<term>Lymphoedème (traitement médicamenteux)</term>
<term>Lymphoedème (étiologie)</term>
<term>Microenvironnement tumoral ()</term>
<term>Néovascularisation physiologique ()</term>
<term>Prolifération cellulaire ()</term>
<term>Protéines suppresseurs de tumeurs (métabolisme)</term>
<term>Protéines à homéodomaine (métabolisme)</term>
<term>Récepteurs à l'interleukine-8 (métabolisme)</term>
<term>Récepteurs à l'interleukine-8A (métabolisme)</term>
<term>Récepteurs à l'interleukine-8B (métabolisme)</term>
<term>Régulation négative ()</term>
<term>Régénération ()</term>
<term>Souris</term>
<term>Souris transgéniques</term>
<term>Trétinoïne (pharmacologie)</term>
<term>Vaisseaux lymphatiques ()</term>
<term>Vaisseaux lymphatiques (anatomopathologie)</term>
<term>Vaisseaux lymphatiques (physiopathologie)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cyclin-Dependent Kinase Inhibitor p57</term>
<term>Homeodomain Proteins</term>
<term>Interleukin-8</term>
<term>Receptors, Interleukin-8</term>
<term>Receptors, Interleukin-8A</term>
<term>Receptors, Interleukin-8B</term>
<term>Tumor Suppressor Proteins</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Complications postopératoires</term>
<term>Lymphoedème</term>
<term>Vaisseaux lymphatiques</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Proliferation</term>
<term>Down-Regulation</term>
<term>Embryonic Development</term>
<term>Endothelial Cells</term>
<term>Lymphangiogenesis</term>
<term>Lymphatic Vessels</term>
<term>Neovascularization, Physiologic</term>
<term>Regeneration</term>
<term>Tumor Microenvironment</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Lymphedema</term>
<term>Postoperative Complications</term>
</keywords>
<keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Lymphedema</term>
<term>Postoperative Complications</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Endothelial Cells</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cellules endothéliales</term>
<term>Inhibiteur p57 de kinase cycline-dépendante</term>
<term>Interleukine-8</term>
<term>Protéines suppresseurs de tumeurs</term>
<term>Protéines à homéodomaine</term>
<term>Récepteurs à l'interleukine-8</term>
<term>Récepteurs à l'interleukine-8A</term>
<term>Récepteurs à l'interleukine-8B</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lymphatic Vessels</term>
<term>Lymphedema</term>
<term>Postoperative Complications</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Facteur de nécrose tumorale alpha</term>
<term>Interleukine-8</term>
<term>Trétinoïne</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Interleukin-8</term>
<term>Tretinoin</term>
<term>Tumor Necrosis Factor-alpha</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Complications postopératoires</term>
<term>Lymphoedème</term>
<term>Vaisseaux lymphatiques</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Lymphatic Vessels</term>
<term>Lymphedema</term>
<term>Postoperative Complications</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Interleukin-8</term>
</keywords>
<keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Complications postopératoires</term>
<term>Lymphoedème</term>
</keywords>
<keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Interleukine-8</term>
</keywords>
<keywords scheme="MESH" qualifier="étiologie" xml:lang="fr"><term>Complications postopératoires</term>
<term>Lymphoedème</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Cells, Cultured</term>
<term>Humans</term>
<term>Mice</term>
<term>Mice, Transgenic</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Cellules cultivées</term>
<term>Cellules endothéliales</term>
<term>Développement embryonnaire</term>
<term>Humains</term>
<term>Lymphangiogenèse</term>
<term>Microenvironnement tumoral</term>
<term>Néovascularisation physiologique</term>
<term>Prolifération cellulaire</term>
<term>Régulation négative</term>
<term>Régénération</term>
<term>Souris</term>
<term>Souris transgéniques</term>
<term>Vaisseaux lymphatiques</term>
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<front><div type="abstract" xml:lang="en">Lymphedema is mainly caused by lymphatic obstruction and manifested as tissue swelling, often in the arms and legs. Lymphedema is one of the most common post-surgical complications in breast cancer patients and presents a painful and disfiguring chronic illness that has few treatment options. Here, we evaluated the therapeutic potential of interleukin (IL)-8 in lymphatic regeneration independent of its pro-inflammatory activity. We found that IL-8 promoted proliferation, tube formation, and migration of lymphatic endothelial cells (LECs) without activating the VEGF signaling. Additionally, IL-8 suppressed the major cell cycle inhibitor CDKN1C/p57(KIP2) by downregulating its positive regulator PROX1, which is known as the master regulator of LEC-differentiation. Animal-based studies such as matrigel plug and cornea micropocket assays demonstrated potent efficacy of IL-8 in activating lymphangiogenesis in vivo. Moreover, we have generated a novel transgenic mouse model (K14-hIL8) that expresses human IL-8 in the skin and then crossed with lymphatic-specific fluorescent (Prox1-GFP) mouse. The resulting double transgenic mice showed that a stable expression of IL-8 could promote embryonic lymphangiogenesis. Moreover, an immunodeficient IL-8-expressing mouse line that was established by crossing K14-hIL8 mice with athymic nude mice displayed an enhanced tumor-associated lymphangiogenesis. Finally, when experimental lymphedema was introduced, K14-hIL8 mice showed an improved amelioration of lymphedema with an increased lymphatic regeneration. Together, we report that IL-8 can activate lymphangiogenesis in vitro and in vivo with a therapeutic efficacy in post-surgical lymphedema.</div>
</front>
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<Title>Angiogenesis</Title>
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<ArticleTitle>Interleukin-8 reduces post-surgical lymphedema formation by promoting lymphatic vessel regeneration.</ArticleTitle>
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</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1007/s10456-012-9297-6</ELocationID>
<Abstract><AbstractText>Lymphedema is mainly caused by lymphatic obstruction and manifested as tissue swelling, often in the arms and legs. Lymphedema is one of the most common post-surgical complications in breast cancer patients and presents a painful and disfiguring chronic illness that has few treatment options. Here, we evaluated the therapeutic potential of interleukin (IL)-8 in lymphatic regeneration independent of its pro-inflammatory activity. We found that IL-8 promoted proliferation, tube formation, and migration of lymphatic endothelial cells (LECs) without activating the VEGF signaling. Additionally, IL-8 suppressed the major cell cycle inhibitor CDKN1C/p57(KIP2) by downregulating its positive regulator PROX1, which is known as the master regulator of LEC-differentiation. Animal-based studies such as matrigel plug and cornea micropocket assays demonstrated potent efficacy of IL-8 in activating lymphangiogenesis in vivo. Moreover, we have generated a novel transgenic mouse model (K14-hIL8) that expresses human IL-8 in the skin and then crossed with lymphatic-specific fluorescent (Prox1-GFP) mouse. The resulting double transgenic mice showed that a stable expression of IL-8 could promote embryonic lymphangiogenesis. Moreover, an immunodeficient IL-8-expressing mouse line that was established by crossing K14-hIL8 mice with athymic nude mice displayed an enhanced tumor-associated lymphangiogenesis. Finally, when experimental lymphedema was introduced, K14-hIL8 mice showed an improved amelioration of lymphedema with an increased lymphatic regeneration. Together, we report that IL-8 can activate lymphangiogenesis in vitro and in vivo with a therapeutic efficacy in post-surgical lymphedema.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Choi</LastName>
<ForeName>Inho</ForeName>
<Initials>I</Initials>
<AffiliationInfo><Affiliation>Department of Surgery, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA 90033, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lee</LastName>
<ForeName>Yong Suk</ForeName>
<Initials>YS</Initials>
</Author>
<Author ValidYN="Y"><LastName>Chung</LastName>
<ForeName>Hee Kyoung</ForeName>
<Initials>HK</Initials>
</Author>
<Author ValidYN="Y"><LastName>Choi</LastName>
<ForeName>Dongwon</ForeName>
<Initials>D</Initials>
</Author>
<Author ValidYN="Y"><LastName>Ecoiffier</LastName>
<ForeName>Tatiana</ForeName>
<Initials>T</Initials>
</Author>
<Author ValidYN="Y"><LastName>Lee</LastName>
<ForeName>Ha Neul</ForeName>
<Initials>HN</Initials>
</Author>
<Author ValidYN="Y"><LastName>Kim</LastName>
<ForeName>Kyu Eui</ForeName>
<Initials>KE</Initials>
</Author>
<Author ValidYN="Y"><LastName>Lee</LastName>
<ForeName>Sunju</ForeName>
<Initials>S</Initials>
</Author>
<Author ValidYN="Y"><LastName>Park</LastName>
<ForeName>Eun Kyung</ForeName>
<Initials>EK</Initials>
</Author>
<Author ValidYN="Y"><LastName>Maeng</LastName>
<ForeName>Yong Sun</ForeName>
<Initials>YS</Initials>
</Author>
<Author ValidYN="Y"><LastName>Kim</LastName>
<ForeName>Nam Yun</ForeName>
<Initials>NY</Initials>
</Author>
<Author ValidYN="Y"><LastName>Ladner</LastName>
<ForeName>Robert D</ForeName>
<Initials>RD</Initials>
</Author>
<Author ValidYN="Y"><LastName>Petasis</LastName>
<ForeName>Nicos A</ForeName>
<Initials>NA</Initials>
</Author>
<Author ValidYN="Y"><LastName>Koh</LastName>
<ForeName>Chester J</ForeName>
<Initials>CJ</Initials>
</Author>
<Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>Lu</ForeName>
<Initials>L</Initials>
</Author>
<Author ValidYN="Y"><LastName>Lenz</LastName>
<ForeName>Heinz-Josef</ForeName>
<Initials>HJ</Initials>
</Author>
<Author ValidYN="Y"><LastName>Hong</LastName>
<ForeName>Young-Kwon</ForeName>
<Initials>YK</Initials>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>R01 EY017392</GrantID>
<Acronym>EY</Acronym>
<Agency>NEI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 HD059762</GrantID>
<Acronym>HD</Acronym>
<Agency>NICHD NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R21 HL082643</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>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2012</Year>
<Month>09</Month>
<Day>04</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>Germany</Country>
<MedlineTA>Angiogenesis</MedlineTA>
<NlmUniqueID>9814575</NlmUniqueID>
<ISSNLinking>0969-6970</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D050761">Cyclin-Dependent Kinase Inhibitor p57</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D018398">Homeodomain Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D016209">Interleukin-8</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D053700">Receptors, Interleukin-8</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D023062">Receptors, Interleukin-8A</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D023063">Receptors, Interleukin-8B</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D014409">Tumor Necrosis Factor-alpha</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D025521">Tumor Suppressor Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C102225">prospero-related homeobox 1 protein</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>5688UTC01R</RegistryNumber>
<NameOfSubstance UI="D014212">Tretinoin</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
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<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D050761" MajorTopicYN="N">Cyclin-Dependent Kinase Inhibitor p57</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015536" MajorTopicYN="N">Down-Regulation</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D047108" MajorTopicYN="N">Embryonic Development</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D042783" MajorTopicYN="N">Endothelial Cells</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018398" MajorTopicYN="N">Homeodomain Proteins</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D016209" MajorTopicYN="N">Interleukin-8</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
<QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D042583" MajorTopicYN="N">Lymphangiogenesis</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D042601" MajorTopicYN="N">Lymphatic Vessels</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
<QualifierName UI="Q000503" MajorTopicYN="Y">physiopathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008209" MajorTopicYN="N">Lymphedema</DescriptorName>
<QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName>
<QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
<QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008822" MajorTopicYN="N">Mice, Transgenic</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018919" MajorTopicYN="N">Neovascularization, Physiologic</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011183" MajorTopicYN="N">Postoperative Complications</DescriptorName>
<QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName>
<QualifierName UI="Q000209" MajorTopicYN="Y">etiology</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
<QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D053700" MajorTopicYN="N">Receptors, Interleukin-8</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D023062" MajorTopicYN="N">Receptors, Interleukin-8A</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D023063" MajorTopicYN="N">Receptors, Interleukin-8B</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012038" MajorTopicYN="Y">Regeneration</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014212" MajorTopicYN="N">Tretinoin</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D059016" MajorTopicYN="N">Tumor Microenvironment</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014409" MajorTopicYN="N">Tumor Necrosis Factor-alpha</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D025521" MajorTopicYN="N">Tumor Suppressor Proteins</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
</MeshHeadingList>
<OtherID Source="NLM">NIHMS406338</OtherID>
<OtherID Source="NLM">PMC4166493</OtherID>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2012</Year>
<Month>03</Month>
<Day>07</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2012</Year>
<Month>08</Month>
<Day>16</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2012</Year>
<Month>9</Month>
<Day>5</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2012</Year>
<Month>9</Month>
<Day>5</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2013</Year>
<Month>6</Month>
<Day>1</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">22945845</ArticleId>
<ArticleId IdType="doi">10.1007/s10456-012-9297-6</ArticleId>
<ArticleId IdType="pmc">PMC4166493</ArticleId>
<ArticleId IdType="mid">NIHMS406338</ArticleId>
</ArticleIdList>
</PubmedData>
</pubmed>
<affiliations><list><country><li>États-Unis</li>
</country>
<region><li>Californie</li>
</region>
<settlement><li>Los Angeles</li>
</settlement>
<orgName><li>Université de Californie du Sud</li>
</orgName>
</list>
<tree><noCountry><name sortKey="Chen, Lu" sort="Chen, Lu" uniqKey="Chen L" first="Lu" last="Chen">Lu Chen</name>
<name sortKey="Choi, Dongwon" sort="Choi, Dongwon" uniqKey="Choi D" first="Dongwon" last="Choi">Dongwon Choi</name>
<name sortKey="Chung, Hee Kyoung" sort="Chung, Hee Kyoung" uniqKey="Chung H" first="Hee Kyoung" last="Chung">Hee Kyoung Chung</name>
<name sortKey="Ecoiffier, Tatiana" sort="Ecoiffier, Tatiana" uniqKey="Ecoiffier T" first="Tatiana" last="Ecoiffier">Tatiana Ecoiffier</name>
<name sortKey="Hong, Young Kwon" sort="Hong, Young Kwon" uniqKey="Hong Y" first="Young-Kwon" last="Hong">Young-Kwon Hong</name>
<name sortKey="Kim, Kyu Eui" sort="Kim, Kyu Eui" uniqKey="Kim K" first="Kyu Eui" last="Kim">Kyu Eui Kim</name>
<name sortKey="Kim, Nam Yun" sort="Kim, Nam Yun" uniqKey="Kim N" first="Nam Yun" last="Kim">Nam Yun Kim</name>
<name sortKey="Koh, Chester J" sort="Koh, Chester J" uniqKey="Koh C" first="Chester J" last="Koh">Chester J. Koh</name>
<name sortKey="Ladner, Robert D" sort="Ladner, Robert D" uniqKey="Ladner R" first="Robert D" last="Ladner">Robert D. Ladner</name>
<name sortKey="Lee, Ha Neul" sort="Lee, Ha Neul" uniqKey="Lee H" first="Ha Neul" last="Lee">Ha Neul Lee</name>
<name sortKey="Lee, Sunju" sort="Lee, Sunju" uniqKey="Lee S" first="Sunju" last="Lee">Sunju Lee</name>
<name sortKey="Lee, Yong Suk" sort="Lee, Yong Suk" uniqKey="Lee Y" first="Yong Suk" last="Lee">Yong Suk Lee</name>
<name sortKey="Lenz, Heinz Josef" sort="Lenz, Heinz Josef" uniqKey="Lenz H" first="Heinz-Josef" last="Lenz">Heinz-Josef Lenz</name>
<name sortKey="Maeng, Yong Sun" sort="Maeng, Yong Sun" uniqKey="Maeng Y" first="Yong Sun" last="Maeng">Yong Sun Maeng</name>
<name sortKey="Park, Eun Kyung" sort="Park, Eun Kyung" uniqKey="Park E" first="Eun Kyung" last="Park">Eun Kyung Park</name>
<name sortKey="Petasis, Nicos A" sort="Petasis, Nicos A" uniqKey="Petasis N" first="Nicos A" last="Petasis">Nicos A. Petasis</name>
</noCountry>
<country name="États-Unis"><region name="Californie"><name sortKey="Choi, Inho" sort="Choi, Inho" uniqKey="Choi I" first="Inho" last="Choi">Inho Choi</name>
</region>
</country>
</tree>
</affiliations>
</record>
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