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Article: Ginsenoside Rb1 inhibits tube-like structure formation of endothelial cells by regulating pigment epithelium-derived factor through the oestrogen β receptor

TitleGinsenoside Rb1 inhibits tube-like structure formation of endothelial cells by regulating pigment epithelium-derived factor through the oestrogen β receptor
Authors
KeywordsAngiogenesis
Endothelial cells
Ginseng
Oestrogen receptor
PEDF
Issue Date2007
PublisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1
Citation
British Journal Of Pharmacology, 2007, v. 152 n. 2, p. 207-215 How to Cite?
AbstractBackground and purpose: Angiogenesis is a crucial step in tumour growth and metastasis. Ginsenoside-Rb1 (Rb1), the major active constituent of ginseng, potently inhibits angiogenesis in vivo and in vitro. However, the underlying mechanism remains unknown. We hypothesized that the potent anti-angiogenic protein, pigment epithelium-derived factor (PEDF), is involved in regulating the anti-angiogenic effects of Rb1. Experimental approaches: Rb1-induced PEDF was determined by real-time PCR and western blot analysis. The anti-angiogenic effects of Rb1 were demonstrated using endothelial cell tube formation assay. Competitive ligand-binding and reporter gene assays were employed to indicate the interaction between Rb1 and the oestrogen receptor (ER). Key results: Rb1 significantly increased the transcription, protein expression and secretion of PEDF. Targeted inhibition of PEDF completely prevented Rb1-induced inhibition of endothelial tube formation, suggesting that the anti-angiogenic effect of Rb1 was PEDF specific. Interestingly, the activation of PEDF occurred via a genomic pathway of ERβ. Competitive ligand-binding assays indicated that Rb1 is a specific agonist of ERβ, but not ERα. Rb1 effectively recruited transcriptional activators and activated an oestrogen-responsive reporter gene. Furthermore, Rb1-mediated PEDF activation and the subsequent inhibition of tube formation were blocked by the ER antagonist ICI 182,780 or transfection of ERβ siRNA, indicating ERβ dependence. Conclusions and implications: Here we show for the first time that the Rb1 suppressed the formation of endothelial tube-like structures through modulation of PEDF via ERβ. These findings demonstrate a novel mechanism of the action of this ginsenoside that may have value in anti-cancer and anti-angiogenesis therapy. © 2007 Nature Publishing Group All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/89213
ISSN
2015 Impact Factor: 5.259
2015 SCImago Journal Rankings: 2.368
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLeung, KWen_HK
dc.contributor.authorCheung, LWTen_HK
dc.contributor.authorPon, YLen_HK
dc.contributor.authorWong, RNSen_HK
dc.contributor.authorMak, NKen_HK
dc.contributor.authorFan, TPPen_HK
dc.contributor.authorAu, SCLen_HK
dc.contributor.authorTombranTink, Jen_HK
dc.contributor.authorWong, ASTen_HK
dc.date.accessioned2010-09-06T09:53:58Z-
dc.date.available2010-09-06T09:53:58Z-
dc.date.issued2007en_HK
dc.identifier.citationBritish Journal Of Pharmacology, 2007, v. 152 n. 2, p. 207-215en_HK
dc.identifier.issn0007-1188en_HK
dc.identifier.urihttp://hdl.handle.net/10722/89213-
dc.description.abstractBackground and purpose: Angiogenesis is a crucial step in tumour growth and metastasis. Ginsenoside-Rb1 (Rb1), the major active constituent of ginseng, potently inhibits angiogenesis in vivo and in vitro. However, the underlying mechanism remains unknown. We hypothesized that the potent anti-angiogenic protein, pigment epithelium-derived factor (PEDF), is involved in regulating the anti-angiogenic effects of Rb1. Experimental approaches: Rb1-induced PEDF was determined by real-time PCR and western blot analysis. The anti-angiogenic effects of Rb1 were demonstrated using endothelial cell tube formation assay. Competitive ligand-binding and reporter gene assays were employed to indicate the interaction between Rb1 and the oestrogen receptor (ER). Key results: Rb1 significantly increased the transcription, protein expression and secretion of PEDF. Targeted inhibition of PEDF completely prevented Rb1-induced inhibition of endothelial tube formation, suggesting that the anti-angiogenic effect of Rb1 was PEDF specific. Interestingly, the activation of PEDF occurred via a genomic pathway of ERβ. Competitive ligand-binding assays indicated that Rb1 is a specific agonist of ERβ, but not ERα. Rb1 effectively recruited transcriptional activators and activated an oestrogen-responsive reporter gene. Furthermore, Rb1-mediated PEDF activation and the subsequent inhibition of tube formation were blocked by the ER antagonist ICI 182,780 or transfection of ERβ siRNA, indicating ERβ dependence. Conclusions and implications: Here we show for the first time that the Rb1 suppressed the formation of endothelial tube-like structures through modulation of PEDF via ERβ. These findings demonstrate a novel mechanism of the action of this ginsenoside that may have value in anti-cancer and anti-angiogenesis therapy. © 2007 Nature Publishing Group All rights reserved.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1en_HK
dc.relation.ispartofBritish Journal of Pharmacologyen_HK
dc.subjectAngiogenesisen_HK
dc.subjectEndothelial cellsen_HK
dc.subjectGinsengen_HK
dc.subjectOestrogen receptoren_HK
dc.subjectPEDFen_HK
dc.titleGinsenoside Rb1 inhibits tube-like structure formation of endothelial cells by regulating pigment epithelium-derived factor through the oestrogen β receptoren_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0007-1188&volume=152&spage=207&epage=215&date=2007&atitle=Ginsenoside+Rb1+inhibits+tube-like+structure+formation+of+endothelial+cells+by+regulating+pigment+epithelium-derived+factor+through+the+oestrogen+beta+receptoren_HK
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.doi10.1038/sj.bjp.0707359en_HK
dc.identifier.pmid17603552-
dc.identifier.scopuseid_2-s2.0-34948887630en_HK
dc.identifier.hkuros130201en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34948887630&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume152en_HK
dc.identifier.issue2en_HK
dc.identifier.spage207en_HK
dc.identifier.epage215en_HK
dc.identifier.isiWOS:000249324800005-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLeung, KW=13106059300en_HK
dc.identifier.scopusauthoridCheung, LWT=14119560800en_HK
dc.identifier.scopusauthoridPon, YL=22235406500en_HK
dc.identifier.scopusauthoridWong, RNS=7402126957en_HK
dc.identifier.scopusauthoridMak, NK=35587830100en_HK
dc.identifier.scopusauthoridFan, TPP=7202528295en_HK
dc.identifier.scopusauthoridAu, SCL=14119361300en_HK
dc.identifier.scopusauthoridTombranTink, J=7003724753en_HK
dc.identifier.scopusauthoridWong, AST=23987963300en_HK

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