9-cis retinoic acid promotes lymphangiogenesis and enhances lymphatic vessel regeneration: therapeutic implications of 9-cis retinoic acid for secondary lymphedema.
Identifieur interne : 002298 ( PubMed/Corpus ); précédent : 002297; suivant : 0022999-cis retinoic acid promotes lymphangiogenesis and enhances lymphatic vessel regeneration: therapeutic implications of 9-cis retinoic acid for secondary lymphedema.
Auteurs : Inho Choi ; Sunju Lee ; Hee Kyoung Chung ; Yong Suk Lee ; Kyu Eui Kim ; Dongwon Choi ; Eun Kyung Park ; Dongyun Yang ; Tatiana Ecoiffier ; John Monahan ; Wen Chen ; Berenice Aguilar ; Ha Neul Lee ; Jaehyuk Yoo ; Chester J. Koh ; Lu Chen ; Alex K. Wong ; Young-Kwon HongSource :
- Circulation [ 1524-4539 ] ; 2012.
English descriptors
- KwdEn :
- Animals, Aurora Kinases, Cell Movement (drug effects), Cell Proliferation (drug effects), Cyclin-Dependent Kinase Inhibitor p27 (genetics), Cyclin-Dependent Kinase Inhibitor p57 (genetics), Endothelial Cells (drug effects), Endothelial Cells (physiology), Fibroblast Growth Factors (physiology), Lymphangiogenesis (drug effects), Lymphatic Vessels (drug effects), Lymphatic Vessels (physiology), Lymphedema (drug therapy), Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Promoter Regions, Genetic, Protein-Serine-Threonine Kinases (genetics), Regeneration (drug effects), Tretinoin (pharmacology), Tretinoin (therapeutic use).
- MESH :
- chemical , genetics : Cyclin-Dependent Kinase Inhibitor p27, Cyclin-Dependent Kinase Inhibitor p57, Protein-Serine-Threonine Kinases.
- chemical , pharmacology : Tretinoin.
- chemical , physiology : Fibroblast Growth Factors.
- chemical , therapeutic use : Tretinoin.
- chemical : Aurora Kinases.
- drug effects : Cell Movement, Cell Proliferation, Endothelial Cells, Lymphangiogenesis, Lymphatic Vessels, Regeneration.
- drug therapy : Lymphedema.
- physiology : Endothelial Cells, Lymphatic Vessels.
- Animals, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Promoter Regions, Genetic.
Abstract
The lymphatic system plays a key role in tissue fluid homeostasis and lymphatic dysfunction caused by genetic defects, or lymphatic vessel obstruction can cause lymphedema, disfiguring tissue swelling often associated with fibrosis and recurrent infections with no available cures to date. In this study, retinoic acids (RAs) were determined to be a potent therapeutic agent that is immediately applicable to reduce secondary lymphedema.
DOI: 10.1161/CIRCULATIONAHA.111.030296
PubMed: 22275501
Links to Exploration step
pubmed:22275501Le document en format XML
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Koh</name></author><author><name sortKey="Chen, Lu" sort="Chen, Lu" uniqKey="Chen L" first="Lu" last="Chen">Lu Chen</name></author><author><name sortKey="Wong, Alex K" sort="Wong, Alex K" uniqKey="Wong A" first="Alex K" last="Wong">Alex K. Wong</name></author><author><name sortKey="Hong, Young Kwon" sort="Hong, Young Kwon" uniqKey="Hong Y" first="Young-Kwon" last="Hong">Young-Kwon Hong</name></author></analytic><series><title level="j">Circulation</title><idno type="eISSN">1524-4539</idno><imprint><date when="2012" type="published">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Aurora Kinases</term><term>Cell Movement (drug effects)</term><term>Cell Proliferation (drug effects)</term><term>Cyclin-Dependent Kinase Inhibitor p27 (genetics)</term><term>Cyclin-Dependent Kinase Inhibitor p57 (genetics)</term><term>Endothelial Cells (drug effects)</term><term>Endothelial Cells (physiology)</term><term>Fibroblast Growth Factors (physiology)</term><term>Lymphangiogenesis (drug effects)</term><term>Lymphatic Vessels (drug effects)</term><term>Lymphatic Vessels (physiology)</term><term>Lymphedema (drug therapy)</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Mice, Inbred C57BL</term><term>Promoter Regions, Genetic</term><term>Protein-Serine-Threonine Kinases (genetics)</term><term>Regeneration (drug effects)</term><term>Tretinoin (pharmacology)</term><term>Tretinoin (therapeutic use)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Cyclin-Dependent Kinase Inhibitor p27</term><term>Cyclin-Dependent Kinase Inhibitor p57</term><term>Protein-Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Tretinoin</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Fibroblast Growth Factors</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Tretinoin</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Aurora Kinases</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Movement</term><term>Cell Proliferation</term><term>Endothelial Cells</term><term>Lymphangiogenesis</term><term>Lymphatic Vessels</term><term>Regeneration</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Lymphedema</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Endothelial Cells</term><term>Lymphatic Vessels</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Mice, Inbred C57BL</term><term>Promoter Regions, Genetic</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The lymphatic system plays a key role in tissue fluid homeostasis and lymphatic dysfunction caused by genetic defects, or lymphatic vessel obstruction can cause lymphedema, disfiguring tissue swelling often associated with fibrosis and recurrent infections with no available cures to date. In this study, retinoic acids (RAs) were determined to be a potent therapeutic agent that is immediately applicable to reduce secondary lymphedema.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">22275501</PMID><DateCreated><Year>2012</Year><Month>02</Month><Day>22</Day></DateCreated><DateCompleted><Year>2012</Year><Month>04</Month><Day>06</Day></DateCompleted><DateRevised><Year>2017</Year><Month>07</Month><Day>26</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1524-4539</ISSN><JournalIssue CitedMedium="Internet"><Volume>125</Volume><Issue>7</Issue><PubDate><Year>2012</Year><Month>Feb</Month><Day>21</Day></PubDate></JournalIssue><Title>Circulation</Title><ISOAbbreviation>Circulation</ISOAbbreviation></Journal><ArticleTitle>9-cis retinoic acid promotes lymphangiogenesis and enhances lymphatic vessel regeneration: therapeutic implications of 9-cis retinoic acid for secondary lymphedema.</ArticleTitle><Pagination><MedlinePgn>872-82</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1161/CIRCULATIONAHA.111.030296</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">The lymphatic system plays a key role in tissue fluid homeostasis and lymphatic dysfunction caused by genetic defects, or lymphatic vessel obstruction can cause lymphedema, disfiguring tissue swelling often associated with fibrosis and recurrent infections with no available cures to date. In this study, retinoic acids (RAs) were determined to be a potent therapeutic agent that is immediately applicable to reduce secondary lymphedema.</AbstractText><AbstractText Label="METHODS AND RESULTS" NlmCategory="RESULTS">We report that RAs promote proliferation, migration, and tube formation of cultured lymphatic endothelial cells by activating fibroblast growth factor receptor signaling. Moreover, RAs control the expression of cell-cycle checkpoint regulators such as p27(Kip1), p57(Kip2), and the aurora kinases through both an Akt-mediated nongenomic action and a transcription-dependent genomic action that is mediated by Prox1, a master regulator of lymphatic development. Moreover, 9-cisRA was found to activate in vivo lymphangiogenesis in animals in mouse trachea, Matrigel plug, and cornea pocket assays. Finally, we demonstrate that 9-cisRA can provide a strong therapeutic efficacy in ameliorating experimental mouse tail lymphedema by enhancing lymphatic vessel regeneration.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">These in vitro and animal studies demonstrate that 9-cisRA potently activates lymphangiogenesis and promotes lymphatic regeneration in an experimental lymphedema model, presenting it as a promising novel therapeutic agent to treat human lymphedema patients.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Choi</LastName><ForeName>Inho</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Department of Surgery, University of Southern California, Norris Comprehensive Cancer Center, 1450 Biggy St, NRT6501, Los Angeles, CA 90033, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Sunju</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Kyoung Chung</LastName><ForeName>Hee</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Suk Lee</LastName><ForeName>Yong</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Eui Kim</LastName><ForeName>Kyu</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Choi</LastName><ForeName>Dongwon</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Park</LastName><ForeName>Eun Kyung</ForeName><Initials>EK</Initials></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Dongyun</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Ecoiffier</LastName><ForeName>Tatiana</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Monahan</LastName><ForeName>John</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Wen</ForeName><Initials>W</Initials></Author><Author ValidYN="Y"><LastName>Aguilar</LastName><ForeName>Berenice</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Ha Neul</ForeName><Initials>HN</Initials></Author><Author ValidYN="Y"><LastName>Yoo</LastName><ForeName>Jaehyuk</ForeName><Initials>J</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>Wong</LastName><ForeName>Alex K</ForeName><Initials>AK</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 HD059762</GrantID><Acronym>HD</Acronym><Agency>NICHD NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R21 HL082643-01A1</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HD059762-05</GrantID><Acronym>HD</Acronym><Agency>NICHD NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HD059762-01</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><Grant><GrantID>R21 HL082643-02</GrantID><Acronym>HL</Acronym><Agency>NHLBI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HD059762-04</GrantID><Acronym>HD</Acronym><Agency>NICHD NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HD059762-02</GrantID><Acronym>HD</Acronym><Agency>NICHD NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HD059762-02S1</GrantID><Acronym>HD</Acronym><Agency>NICHD NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 EY017392</GrantID><Acronym>EY</Acronym><Agency>NEI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 HD059762-03</GrantID><Acronym>HD</Acronym><Agency>NICHD 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>01</Month><Day>24</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Circulation</MedlineTA><NlmUniqueID>0147763</NlmUniqueID><ISSNLinking>0009-7322</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C493961">Cdkn1b protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C493965">Cdkn1c protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050761">Cyclin-Dependent Kinase Inhibitor p57</NameOfSubstance></Chemical><Chemical><RegistryNumber>147604-94-2</RegistryNumber><NameOfSubstance UI="D050760">Cyclin-Dependent Kinase Inhibitor p27</NameOfSubstance></Chemical><Chemical><RegistryNumber>1UA8E65KDZ</RegistryNumber><NameOfSubstance UI="C103303">alitretinoin</NameOfSubstance></Chemical><Chemical><RegistryNumber>5688UTC01R</RegistryNumber><NameOfSubstance UI="D014212">Tretinoin</NameOfSubstance></Chemical><Chemical><RegistryNumber>62031-54-3</RegistryNumber><NameOfSubstance UI="D005346">Fibroblast Growth Factors</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D064127">Aurora Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 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