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Article: Ginsenoside-Rg1 induces angiogenesis via non-genomic crosstalk of glucocorticoid receptor and fibroblast growth factor receptor-1

TitleGinsenoside-Rg1 induces angiogenesis via non-genomic crosstalk of glucocorticoid receptor and fibroblast growth factor receptor-1
Authors
KeywordsENOS
Ginseng
HUVEC
PI3K/Akt
Signalling
Issue Date2011
PublisherOxford University Press. The Journal's web site is located at http://cardiovascres.oxfordjournals.org
Citation
Cardiovascular Research, 2011, v. 89 n. 2, p. 419-425 How to Cite?
AbstractAimsGinsenoside-Rg1, the most prevalent active constituent of Panax ginseng, has been shown to possess potent pro-angiogenic properties and therefore poses special interest for the development as a novel modality for angiotherapy. Rg1 can activate the glucocorticoid receptor (GR). However, the mechanism that transmits these pro-angiogenic effects is still unclear. Methods and resultsBy using human umbilical vein endothelial cells (HUVECs), we show for the first time that in the presence of Rg1, GR and fibroblast growth factor receptor-1 (FGFR-1) cooperate to activate a non-genomic signalling cascade that results in angiogenic activity. The activation of FGFR-1 by Rg1 was blocked by the GR antagonist RU486. Depletion of FGFR-1 expression or inhibition of its activity using small interfering RNA and small molecule inhibitor, respectively, significantly inhibited Rg1-induced phosphatidylinositol 3-kinase/Akt phosphorylation and subsequent endothelial nitric oxide synthase activation and angiogenic tube formation, confirming that the effect was FGFR-1 specific. On exploring how GR might regulate the activation of FGFR-1, we found that GR-mediated FGFR-1 activation was ligand-independent. In addition, we have shown that FGFR-1 regulation by GR was associated with GR/FGFR-1 complex formation. ConclusionThis study provides important new insights into the mechanism regarding the beneficial effects of Rg1 on angiogenesis. We propose that Rg1 could be a novel prototype of nutraceutical that can induce therapeutic angiogenesis. © 2010 The Author.
Persistent Identifierhttp://hdl.handle.net/10722/136255
ISSN
2015 Impact Factor: 5.465
2015 SCImago Journal Rankings: 2.897
ISI Accession Number ID
Funding AgencyGrant Number
Hong Kong Research Grant CouncilHKBU 1/06C
HKU
Funding Information:

This work was supported by grants from the Hong Kong Research Grant Council HKBU 1/06C and the HKU Outstanding Young Researcher Award to A.S.T.W.

References
Grants

 

DC FieldValueLanguage
dc.contributor.authorCheung, LWTen_HK
dc.contributor.authorLeung, KWen_HK
dc.contributor.authorWong, CKCen_HK
dc.contributor.authorWong, RNSen_HK
dc.contributor.authorWong, ASTen_HK
dc.date.accessioned2011-07-27T02:11:45Z-
dc.date.available2011-07-27T02:11:45Z-
dc.date.issued2011en_HK
dc.identifier.citationCardiovascular Research, 2011, v. 89 n. 2, p. 419-425en_HK
dc.identifier.issn0008-6363en_HK
dc.identifier.urihttp://hdl.handle.net/10722/136255-
dc.description.abstractAimsGinsenoside-Rg1, the most prevalent active constituent of Panax ginseng, has been shown to possess potent pro-angiogenic properties and therefore poses special interest for the development as a novel modality for angiotherapy. Rg1 can activate the glucocorticoid receptor (GR). However, the mechanism that transmits these pro-angiogenic effects is still unclear. Methods and resultsBy using human umbilical vein endothelial cells (HUVECs), we show for the first time that in the presence of Rg1, GR and fibroblast growth factor receptor-1 (FGFR-1) cooperate to activate a non-genomic signalling cascade that results in angiogenic activity. The activation of FGFR-1 by Rg1 was blocked by the GR antagonist RU486. Depletion of FGFR-1 expression or inhibition of its activity using small interfering RNA and small molecule inhibitor, respectively, significantly inhibited Rg1-induced phosphatidylinositol 3-kinase/Akt phosphorylation and subsequent endothelial nitric oxide synthase activation and angiogenic tube formation, confirming that the effect was FGFR-1 specific. On exploring how GR might regulate the activation of FGFR-1, we found that GR-mediated FGFR-1 activation was ligand-independent. In addition, we have shown that FGFR-1 regulation by GR was associated with GR/FGFR-1 complex formation. ConclusionThis study provides important new insights into the mechanism regarding the beneficial effects of Rg1 on angiogenesis. We propose that Rg1 could be a novel prototype of nutraceutical that can induce therapeutic angiogenesis. © 2010 The Author.en_HK
dc.languageengen_US
dc.publisherOxford University Press. The Journal's web site is located at http://cardiovascres.oxfordjournals.orgen_HK
dc.relation.ispartofCardiovascular Researchen_HK
dc.subjectENOSen_HK
dc.subjectGinsengen_HK
dc.subjectHUVECen_HK
dc.subjectPI3K/Akten_HK
dc.subjectSignallingen_HK
dc.subject.meshAngiogenesis Inducing Agents - pharmacology-
dc.subject.meshEndothelial Cells - drug effects - metabolism-
dc.subject.meshGinsenosides - pharmacology-
dc.subject.meshNeovascularization, Physiologic - drug effects-
dc.subject.meshReceptor Cross-Talk - drug effects-
dc.titleGinsenoside-Rg1 induces angiogenesis via non-genomic crosstalk of glucocorticoid receptor and fibroblast growth factor receptor-1en_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0008-6363&volume=89&issue=2&spage=419&epage=425&date=2011&atitle=Ginsenoside-Rg1+induces+angiogenesis+via+non-genomic+cross-talk+of+glucocorticoid+receptor+and+fibroblast+growth+factor+receptor-1-
dc.identifier.emailLeung, KW: kwleung1@hku.hken_HK
dc.identifier.emailWong, AST: awong1@hkucc.hku.hken_HK
dc.identifier.authorityLeung, KW=rp01674en_HK
dc.identifier.authorityWong, AST=rp00805en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1093/cvr/cvq300en_HK
dc.identifier.pmid20855522-
dc.identifier.scopuseid_2-s2.0-78751471555en_HK
dc.identifier.hkuros188957en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-78751471555&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume89en_HK
dc.identifier.issue2en_HK
dc.identifier.spage419en_HK
dc.identifier.epage425en_HK
dc.identifier.isiWOS:000286216900022-
dc.publisher.placeUnited Kingdomen_HK
dc.relation.projectGinsenosides as functional ligands of steroid hormone receptors: from ligand-receptor interaction to cellular homeostasis-
dc.identifier.scopusauthoridCheung, LWT=14119560800en_HK
dc.identifier.scopusauthoridLeung, KW=13106059300en_HK
dc.identifier.scopusauthoridWong, CKC=35276549400en_HK
dc.identifier.scopusauthoridWong, RNS=7402126957en_HK
dc.identifier.scopusauthoridWong, AST=23987963300en_HK

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