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Article: A novel function for dendritic cell: clearance of VEGF via VEGF receptor-1

TitleA novel function for dendritic cell: clearance of VEGF via VEGF receptor-1
Authors
Issue Date2009
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ybbrc
Citation
Biochemical And Biophysical Research Communications, 2009, v. 380 n. 2, p. 243-248 How to Cite?
AbstractIt Has Been Reported That The Plasma Levels Of Vegf In Tumor Patients Decreased During Dendritic Cell (Dc)-Based Immunotherapy, But The Underlying Mechanism Remains Unclear. Our Current Report Demonstrates That Vegf Levels Were Significantly Decreased In The Supernatants Of Dcs Incubated With Rhvegf Or Tumor Conditioned Medium (Tcm) While The Intracellular Vegf In Dcs Was Increased. The Increased Intracellular Vegf Was Not Due To The De Novo Vegf Synthesis By Dcs Because Exogenous Vegf Inhibited The Mrna Expression Of Vegf In Dcs. More Direct Evidence Was Provided To Demonstrate That Cy3-Labeled Vegf Could Be Internalized By Dcs Specifically And Efficiently. In Addition, The Activity Of Dcs To Internalize Vegf Was Abolished By Neutralizing Antibody Against Vegf Receptor-1 (Flt-1) And Inhibitors Of Endocytosis Such As Carbonyl Cyanide M-Chlorophenyl Hydrazone (Cccp) And Genistein. This Study Highlights A Novel Function Of Dcs And Allows A Better Understanding Of The Dc-Vegf Interaction. © 2009 Elsevier Inc. All Rights Reserved.
Persistent Identifierhttp://hdl.handle.net/10722/59947
ISSN
2015 Impact Factor: 2.371
2015 SCImago Journal Rankings: 1.152
ISI Accession Number ID
Funding AgencyGrant Number
Hong Kong Research Grants CouncilHKU 7250/02M
National Science FoundationDMS0714589
National Institutes of HealthR01-GM072611
Funding Information:

This research was supported by Hong Kong Research Grants Council (HKU 7250/02M), National Science Foundation (DMS0714589) and National Institutes of Health (R01-GM072611).

References

 

DC FieldValueLanguage
dc.contributor.authorXie, Yen_HK
dc.contributor.authorFan, JQen_HK
dc.contributor.authorChen, JHen_HK
dc.contributor.authorHuang, FPen_HK
dc.contributor.authorCao, Ben_HK
dc.contributor.authorTam, PKHen_HK
dc.contributor.authorRen, Yen_HK
dc.date.accessioned2010-05-31T04:00:41Z-
dc.date.available2010-05-31T04:00:41Z-
dc.date.issued2009en_HK
dc.identifier.citationBiochemical And Biophysical Research Communications, 2009, v. 380 n. 2, p. 243-248en_US
dc.identifier.issn0006-291Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/59947-
dc.description.abstractIt Has Been Reported That The Plasma Levels Of Vegf In Tumor Patients Decreased During Dendritic Cell (Dc)-Based Immunotherapy, But The Underlying Mechanism Remains Unclear. Our Current Report Demonstrates That Vegf Levels Were Significantly Decreased In The Supernatants Of Dcs Incubated With Rhvegf Or Tumor Conditioned Medium (Tcm) While The Intracellular Vegf In Dcs Was Increased. The Increased Intracellular Vegf Was Not Due To The De Novo Vegf Synthesis By Dcs Because Exogenous Vegf Inhibited The Mrna Expression Of Vegf In Dcs. More Direct Evidence Was Provided To Demonstrate That Cy3-Labeled Vegf Could Be Internalized By Dcs Specifically And Efficiently. In Addition, The Activity Of Dcs To Internalize Vegf Was Abolished By Neutralizing Antibody Against Vegf Receptor-1 (Flt-1) And Inhibitors Of Endocytosis Such As Carbonyl Cyanide M-Chlorophenyl Hydrazone (Cccp) And Genistein. This Study Highlights A Novel Function Of Dcs And Allows A Better Understanding Of The Dc-Vegf Interaction. © 2009 Elsevier Inc. All Rights Reserved.en_US
dc.languageengen_HK
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ybbrcen_HK
dc.relation.ispartofBiochemical and Biophysical Research Communicationsen_HK
dc.titleA novel function for dendritic cell: clearance of VEGF via VEGF receptor-1en_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0006-291X&volume=380&spage=243&epage=248&date=2009&atitle=A+novel+function+for+dendritic+cell:+clearance+of+VEGF+via+VEGF+receptor-1en_HK
dc.identifier.emailTam, PKH: paultam@hkucc.hku.hken_HK
dc.identifier.emailRen, Y: yren@hkucc.hku.hken_HK
dc.identifier.authorityTam, PKH=rp00060en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.bbrc.2009.01.043en_US
dc.identifier.pmid19167346-
dc.identifier.scopuseid_2-s2.0-60349111039en_US
dc.identifier.hkuros155040en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-60349111039&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume380en_US
dc.identifier.issue2en_US
dc.identifier.spage243en_US
dc.identifier.epage248en_US
dc.identifier.isiWOS:000263742200007-

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