Dimethylfumarate effectively inhibits lymphangiogenesis via p21 induction and G1 cell cycle arrest.
Identifieur interne : 000B02 ( PubMed/Curation ); précédent : 000B01; suivant : 000B03Dimethylfumarate effectively inhibits lymphangiogenesis via p21 induction and G1 cell cycle arrest.
Auteurs : Eva Maria Valesky [Allemagne] ; Igor Hrgovic [Allemagne] ; Monika Doll [Allemagne] ; Xiao-Fan Wang [États-Unis] ; Andreas Pinter [Allemagne] ; Johannes Kleemann [Allemagne] ; Roland Kaufmann [Allemagne] ; Stefan Kippenberger [Allemagne] ; Markus Meissner [Allemagne]Source :
- Experimental dermatology [ 1600-0625 ] ; 2016.
Descripteurs français
- KwdFr :
- ARN messager (métabolisme), Apoptose, Cycline A (métabolisme), Cycline D1 (métabolisme), Cytométrie en flux, Fumarate de diméthyle (), Humains, Immunosuppresseurs (), Inhibiteur p21 de kinase cycline-dépendante (métabolisme), Lignée cellulaire, Lymphangiogenèse (physiologie), Maturation post-traductionnelle des protéines, Maturation post-transcriptionnelle des ARN, Phase G1, Points de contrôle du cycle cellulaire, Prolifération cellulaire, Séparation cellulaire.
- MESH :
- métabolisme : ARN messager, Cycline A, Cycline D1, Inhibiteur p21 de kinase cycline-dépendante.
- physiologie : Lymphangiogenèse.
- Apoptose, Cytométrie en flux, Fumarate de diméthyle, Humains, Immunosuppresseurs, Lignée cellulaire, Maturation post-traductionnelle des protéines, Maturation post-transcriptionnelle des ARN, Phase G1, Points de contrôle du cycle cellulaire, Prolifération cellulaire, Séparation cellulaire.
English descriptors
- KwdEn :
- Apoptosis, Cell Cycle Checkpoints, Cell Line, Cell Proliferation, Cell Separation, Cyclin A (metabolism), Cyclin D1 (metabolism), Cyclin-Dependent Kinase Inhibitor p21 (metabolism), Dimethyl Fumarate (chemistry), Flow Cytometry, G1 Phase, Humans, Immunosuppressive Agents (chemistry), Lymphangiogenesis (physiology), Protein Processing, Post-Translational, RNA Processing, Post-Transcriptional, RNA, Messenger (metabolism).
- MESH :
- chemical , chemistry : Dimethyl Fumarate, Immunosuppressive Agents.
- chemical , metabolism : Cyclin A, Cyclin D1, Cyclin-Dependent Kinase Inhibitor p21, RNA, Messenger.
- physiology : Lymphangiogenesis.
- Apoptosis, Cell Cycle Checkpoints, Cell Line, Cell Proliferation, Cell Separation, Flow Cytometry, G1 Phase, Humans, Protein Processing, Post-Translational, RNA Processing, Post-Transcriptional.
Abstract
Different pathologies, such as lymphoedema, cancer or psoriasis, are associated with abnormal lymphatic vessel formation. Therefore, influencing lymphangiogenesis is an interesting target. Recent evidence suggests that dimethylfumarate (DMF), an antipsoriatic agent, might have antitumorigenic and antilymphangiogenic properties. To prove this assumption, we performed proliferation and functional assays with primary human dermal lymphendothelial cells (DLEC). We could demonstrated that DMF suppresses DLEC proliferation and formation of capillary-like structures. Underlying apoptotic mechanisms could be ruled out. Cell cycle analysis demonstrated a pronounced G1-arrest. Further evaluations revealed increases in p21 expression. In addition, DMF suppressed Cyclin D1 and Cyclin A expression in a concentration-dependent manner. p21 knockdown experiments demonstrated a p21-dependent mechanism of regulation. Further analysis showed an increased p21 mRNA expression after DMF treatment. This transcriptional regulation was enforced by post-transcriptional and post-translational mechanisms. In addition, we could demonstrate that the combination of a proteasomal inhibitor and DMF superinduced the p21 expression. Hence, DMF is a new antilymphangiogenic compound and might be used in various illnesses associated with increased lymphangiogenesis.
DOI: 10.1111/exd.12907
PubMed: 26663097
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I" first="Igor" last="Hrgovic">Igor Hrgovic</name><affiliation wicri:level="1"><nlm:affiliation>Department of Dermatology, Venereology and Allergology, Goethe-University, Frankfurt am Main, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Dermatology, Venereology and Allergology, Goethe-University, Frankfurt am Main</wicri:regionArea></affiliation></author><author><name sortKey="Doll, Monika" sort="Doll, Monika" uniqKey="Doll M" first="Monika" last="Doll">Monika Doll</name><affiliation wicri:level="1"><nlm:affiliation>Department of Dermatology, Venereology and Allergology, Goethe-University, Frankfurt am Main, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Dermatology, Venereology and Allergology, Goethe-University, Frankfurt am Main</wicri:regionArea></affiliation></author><author><name sortKey="Wang, Xiao Fan" sort="Wang, Xiao Fan" uniqKey="Wang X" first="Xiao-Fan" 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first="Stefan" last="Kippenberger">Stefan Kippenberger</name><affiliation wicri:level="1"><nlm:affiliation>Department of Dermatology, Venereology and Allergology, Goethe-University, Frankfurt am Main, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Dermatology, Venereology and Allergology, Goethe-University, Frankfurt am Main</wicri:regionArea></affiliation></author><author><name sortKey="Meissner, Markus" sort="Meissner, Markus" uniqKey="Meissner M" first="Markus" last="Meissner">Markus Meissner</name><affiliation wicri:level="1"><nlm:affiliation>Department of Dermatology, Venereology and Allergology, Goethe-University, Frankfurt am Main, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Dermatology, Venereology and Allergology, Goethe-University, Frankfurt am Main</wicri:regionArea></affiliation></author></analytic><series><title level="j">Experimental dermatology</title><idno type="eISSN">1600-0625</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Apoptosis</term><term>Cell Cycle Checkpoints</term><term>Cell Line</term><term>Cell Proliferation</term><term>Cell Separation</term><term>Cyclin A (metabolism)</term><term>Cyclin D1 (metabolism)</term><term>Cyclin-Dependent Kinase Inhibitor p21 (metabolism)</term><term>Dimethyl Fumarate (chemistry)</term><term>Flow Cytometry</term><term>G1 Phase</term><term>Humans</term><term>Immunosuppressive Agents (chemistry)</term><term>Lymphangiogenesis (physiology)</term><term>Protein Processing, Post-Translational</term><term>RNA Processing, Post-Transcriptional</term><term>RNA, Messenger (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ARN messager (métabolisme)</term><term>Apoptose</term><term>Cycline A (métabolisme)</term><term>Cycline D1 (métabolisme)</term><term>Cytométrie en flux</term><term>Fumarate de diméthyle ()</term><term>Humains</term><term>Immunosuppresseurs ()</term><term>Inhibiteur p21 de kinase cycline-dépendante (métabolisme)</term><term>Lignée cellulaire</term><term>Lymphangiogenèse (physiologie)</term><term>Maturation post-traductionnelle des protéines</term><term>Maturation post-transcriptionnelle des ARN</term><term>Phase G1</term><term>Points de contrôle du cycle cellulaire</term><term>Prolifération cellulaire</term><term>Séparation cellulaire</term></keywords><keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Dimethyl Fumarate</term><term>Immunosuppressive Agents</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cyclin A</term><term>Cyclin D1</term><term>Cyclin-Dependent Kinase Inhibitor p21</term><term>RNA, Messenger</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>ARN messager</term><term>Cycline A</term><term>Cycline D1</term><term>Inhibiteur p21 de kinase cycline-dépendante</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Lymphangiogenèse</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Lymphangiogenesis</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Apoptosis</term><term>Cell Cycle Checkpoints</term><term>Cell Line</term><term>Cell Proliferation</term><term>Cell Separation</term><term>Flow Cytometry</term><term>G1 Phase</term><term>Humans</term><term>Protein Processing, Post-Translational</term><term>RNA Processing, Post-Transcriptional</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Apoptose</term><term>Cytométrie en flux</term><term>Fumarate de diméthyle</term><term>Humains</term><term>Immunosuppresseurs</term><term>Lignée cellulaire</term><term>Maturation post-traductionnelle des protéines</term><term>Maturation post-transcriptionnelle des ARN</term><term>Phase G1</term><term>Points de contrôle du cycle cellulaire</term><term>Prolifération cellulaire</term><term>Séparation cellulaire</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Different pathologies, such as lymphoedema, cancer or psoriasis, are associated with abnormal lymphatic vessel formation. Therefore, influencing lymphangiogenesis is an interesting target. Recent evidence suggests that dimethylfumarate (DMF), an antipsoriatic agent, might have antitumorigenic and antilymphangiogenic properties. To prove this assumption, we performed proliferation and functional assays with primary human dermal lymphendothelial cells (DLEC). We could demonstrated that DMF suppresses DLEC proliferation and formation of capillary-like structures. Underlying apoptotic mechanisms could be ruled out. Cell cycle analysis demonstrated a pronounced G1-arrest. Further evaluations revealed increases in p21 expression. In addition, DMF suppressed Cyclin D1 and Cyclin A expression in a concentration-dependent manner. p21 knockdown experiments demonstrated a p21-dependent mechanism of regulation. Further analysis showed an increased p21 mRNA expression after DMF treatment. This transcriptional regulation was enforced by post-transcriptional and post-translational mechanisms. In addition, we could demonstrate that the combination of a proteasomal inhibitor and DMF superinduced the p21 expression. Hence, DMF is a new antilymphangiogenic compound and might be used in various illnesses associated with increased lymphangiogenesis.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26663097</PMID><DateCreated><Year>2016</Year><Month>03</Month><Day>12</Day></DateCreated><DateCompleted><Year>2017</Year><Month>03</Month><Day>07</Day></DateCompleted><DateRevised><Year>2017</Year><Month>03</Month><Day>07</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1600-0625</ISSN><JournalIssue CitedMedium="Internet"><Volume>25</Volume><Issue>3</Issue><PubDate><Year>2016</Year><Month>Mar</Month></PubDate></JournalIssue><Title>Experimental dermatology</Title><ISOAbbreviation>Exp. Dermatol.</ISOAbbreviation></Journal><ArticleTitle>Dimethylfumarate effectively inhibits lymphangiogenesis via p21 induction and G1 cell cycle arrest.</ArticleTitle><Pagination><MedlinePgn>200-5</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/exd.12907</ELocationID><Abstract><AbstractText>Different pathologies, such as lymphoedema, cancer or psoriasis, are associated with abnormal lymphatic vessel formation. Therefore, influencing lymphangiogenesis is an interesting target. Recent evidence suggests that dimethylfumarate (DMF), an antipsoriatic agent, might have antitumorigenic and antilymphangiogenic properties. To prove this assumption, we performed proliferation and functional assays with primary human dermal lymphendothelial cells (DLEC). We could demonstrated that DMF suppresses DLEC proliferation and formation of capillary-like structures. Underlying apoptotic mechanisms could be ruled out. Cell cycle analysis demonstrated a pronounced G1-arrest. Further evaluations revealed increases in p21 expression. In addition, DMF suppressed Cyclin D1 and Cyclin A expression in a concentration-dependent manner. p21 knockdown experiments demonstrated a p21-dependent mechanism of regulation. Further analysis showed an increased p21 mRNA expression after DMF treatment. This transcriptional regulation was enforced by post-transcriptional and post-translational mechanisms. In addition, we could demonstrate that the combination of a proteasomal inhibitor and DMF superinduced the p21 expression. Hence, DMF is a new antilymphangiogenic compound and might be used in various illnesses associated with increased lymphangiogenesis.</AbstractText><CopyrightInformation>© 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Valesky</LastName><ForeName>Eva Maria</ForeName><Initials>EM</Initials><AffiliationInfo><Affiliation>Department of Dermatology, Venereology and Allergology, Goethe-University, Frankfurt am Main, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hrgovic</LastName><ForeName>Igor</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Department of Dermatology, Venereology and Allergology, Goethe-University, Frankfurt am Main, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Doll</LastName><ForeName>Monika</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Dermatology, Venereology and Allergology, Goethe-University, Frankfurt am Main, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wang</LastName><ForeName>Xiao-Fan</ForeName><Initials>XF</Initials><AffiliationInfo><Affiliation>Department of Pharmacology & Cancer Biology, Duke University School of Medicine, Durham, NC, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Pinter</LastName><ForeName>Andreas</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Dermatology, Venereology and Allergology, Goethe-University, Frankfurt am Main, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kleemann</LastName><ForeName>Johannes</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Dermatology, Venereology and Allergology, Goethe-University, Frankfurt am Main, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kaufmann</LastName><ForeName>Roland</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Dermatology, Venereology and Allergology, Goethe-University, Frankfurt am Main, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kippenberger</LastName><ForeName>Stefan</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Dermatology, Venereology and Allergology, Goethe-University, Frankfurt am Main, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Meissner</LastName><ForeName>Markus</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Dermatology, Venereology and Allergology, Goethe-University, Frankfurt am Main, Germany.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>02</Month><Day>10</Day></ArticleDate></Article><MedlineJournalInfo><Country>Denmark</Country><MedlineTA>Exp Dermatol</MedlineTA><NlmUniqueID>9301549</NlmUniqueID><ISSNLinking>0906-6705</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C493956">CDKN1A protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019925">Cyclin A</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050759">Cyclin-Dependent Kinase Inhibitor p21</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007166">Immunosuppressive Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012333">RNA, Messenger</NameOfSubstance></Chemical><Chemical><RegistryNumber>136601-57-5</RegistryNumber><NameOfSubstance UI="D019938">Cyclin D1</NameOfSubstance></Chemical><Chemical><RegistryNumber>FO2303MNI2</RegistryNumber><NameOfSubstance UI="D000069462">Dimethyl Fumarate</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D059447" MajorTopicYN="Y">Cell Cycle Checkpoints</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002460" MajorTopicYN="N">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002469" MajorTopicYN="N">Cell Separation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019925" MajorTopicYN="N">Cyclin A</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019938" MajorTopicYN="N">Cyclin D1</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050759" MajorTopicYN="N">Cyclin-Dependent Kinase Inhibitor p21</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000069462" MajorTopicYN="N">Dimethyl Fumarate</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="Y">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005434" MajorTopicYN="N">Flow Cytometry</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016193" MajorTopicYN="N">G1 Phase</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007166" MajorTopicYN="N">Immunosuppressive Agents</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D042583" MajorTopicYN="N">Lymphangiogenesis</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011499" MajorTopicYN="N">Protein Processing, Post-Translational</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012323" MajorTopicYN="N">RNA Processing, Post-Transcriptional</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012333" MajorTopicYN="N">RNA, Messenger</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">dimethylfumarate</Keyword><Keyword MajorTopicYN="N">lymphangiogenesis</Keyword><Keyword MajorTopicYN="N">lymphendothelial</Keyword><Keyword MajorTopicYN="N">p21</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="accepted"><Year>2015</Year><Month>12</Month><Day>04</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>12</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>12</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>3</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">26663097</ArticleId><ArticleId IdType="doi">10.1111/exd.12907</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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