Dimethylfumarate effectively inhibits lymphangiogenesis via p21 induction and G1 cell cycle arrest.
Identifieur interne : 000B02 ( PubMed/Corpus ); précédent : 000B01; suivant : 000B03Dimethylfumarate effectively inhibits lymphangiogenesis via p21 induction and G1 cell cycle arrest.
Auteurs : Eva Maria Valesky ; Igor Hrgovic ; Monika Doll ; Xiao-Fan Wang ; Andreas Pinter ; Johannes Kleemann ; Roland Kaufmann ; Stefan Kippenberger ; Markus MeissnerSource :
- Experimental dermatology [ 1600-0625 ] ; 2016.
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
Links to Exploration step
pubmed:26663097Le document en format XML
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<affiliation><nlm:affiliation>Department of Dermatology, Venereology and Allergology, Goethe-University, Frankfurt am Main, Germany.</nlm:affiliation>
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<author><name sortKey="Doll, Monika" sort="Doll, Monika" uniqKey="Doll M" first="Monika" last="Doll">Monika Doll</name>
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<author><name sortKey="Wang, Xiao Fan" sort="Wang, Xiao Fan" uniqKey="Wang X" first="Xiao-Fan" last="Wang">Xiao-Fan Wang</name>
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<author><name sortKey="Kleemann, Johannes" sort="Kleemann, Johannes" uniqKey="Kleemann J" first="Johannes" last="Kleemann">Johannes Kleemann</name>
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<author><name sortKey="Kaufmann, Roland" sort="Kaufmann, Roland" uniqKey="Kaufmann R" first="Roland" last="Kaufmann">Roland Kaufmann</name>
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<author><name sortKey="Kippenberger, Stefan" sort="Kippenberger, Stefan" uniqKey="Kippenberger S" first="Stefan" last="Kippenberger">Stefan Kippenberger</name>
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<author><name sortKey="Meissner, Markus" sort="Meissner, Markus" uniqKey="Meissner M" first="Markus" last="Meissner">Markus Meissner</name>
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<author><name sortKey="Doll, Monika" sort="Doll, Monika" uniqKey="Doll M" first="Monika" last="Doll">Monika Doll</name>
<affiliation><nlm:affiliation>Department of Dermatology, Venereology and Allergology, Goethe-University, Frankfurt am Main, Germany.</nlm:affiliation>
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<author><name sortKey="Wang, Xiao Fan" sort="Wang, Xiao Fan" uniqKey="Wang X" first="Xiao-Fan" last="Wang">Xiao-Fan Wang</name>
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<series><title level="j">Experimental dermatology</title>
<idno type="eISSN">1600-0625</idno>
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<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="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>
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<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Lymphangiogenesis</term>
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<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>
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<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>
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<Title>Experimental dermatology</Title>
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<ArticleTitle>Dimethylfumarate effectively inhibits lymphangiogenesis via p21 induction and G1 cell cycle arrest.</ArticleTitle>
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<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>
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<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Valesky</LastName>
<ForeName>Eva Maria</ForeName>
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<AffiliationInfo><Affiliation>Department of Dermatology, Venereology and Allergology, Goethe-University, Frankfurt am Main, Germany.</Affiliation>
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<ForeName>Stefan</ForeName>
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<AffiliationInfo><Affiliation>Department of Dermatology, Venereology and Allergology, Goethe-University, Frankfurt am Main, Germany.</Affiliation>
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<Author ValidYN="Y"><LastName>Meissner</LastName>
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<AffiliationInfo><Affiliation>Department of Dermatology, Venereology and Allergology, Goethe-University, Frankfurt am Main, Germany.</Affiliation>
</AffiliationInfo>
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<Month>02</Month>
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<MedlineJournalInfo><Country>Denmark</Country>
<MedlineTA>Exp Dermatol</MedlineTA>
<NlmUniqueID>9301549</NlmUniqueID>
<ISSNLinking>0906-6705</ISSNLinking>
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<MeshHeading><DescriptorName UI="D012323" MajorTopicYN="N">RNA Processing, Post-Transcriptional</DescriptorName>
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<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">dimethylfumarate</Keyword>
<Keyword MajorTopicYN="N">lymphangiogenesis</Keyword>
<Keyword MajorTopicYN="N">lymphendothelial</Keyword>
<Keyword MajorTopicYN="N">p21</Keyword>
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