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Article: Up-regulation of vascular endothelial growth factor (VEGF) in small-for-size liver grafts enhances macrophage activities through VEGF receptor 2-dependent pathway

TitleUp-regulation of vascular endothelial growth factor (VEGF) in small-for-size liver grafts enhances macrophage activities through VEGF receptor 2-dependent pathway
Authors
Issue Date2004
PublisherAmerican Association of Immunologists. The Journal's web site is located at http://www.jimmunol.org
Citation
Journal Of Immunology, 2004, v. 173 n. 4, p. 2507-2515 How to Cite?
AbstractThis study aims to investigate the potential role of vascular endothelial growth factor (VEGF) and VEGF-R2 (fetal liver kinase (Flk)-1) in mediating macrophage activities in small-for-size liver transplantation. A rat orthotopic liver transplantation model was performed using either whole, 50, or 30% liver grafts (both 50 and 30% were regarded as small-for-size) in syngeneic or allogeneic combinations, respectively. Firstly, the mRNA and protein levels of VEGF and Flk-1 in liver grafts were detected by RT-PCR and Western blot, and the number of Flk-1 + macrophages (labeled by ED1) was determined by flow cytometry. It was found that the small-for-size isografts and allografts presented higher levels of VEGF and Flk-1 expression than the whole isograft and allograft. In addition, a higher number of Flk-1 +ED1 + cells were detected in the small-for-size isografts and allografts than the whole isograft and allograft. Secondly, our study revealed that macrophage cell lines did not initially express detectable Flk-1, but could be induced by VEGF, and the inducible expression of Flk-1 in macrophages was related to their migration and proliferation activities. Finally, our study demonstrated that the induction of Flk-1 expression on macrophages by VEGF was associated with the expression of NF-κB and heat shock protein 90. In conclusion, the present study showed that the up-regulated expression of VEGF and its interaction with Flk-1 in small-for-size liver grafts might facilitate the activities of macrophages.
Persistent Identifierhttp://hdl.handle.net/10722/49345
ISSN
2015 Impact Factor: 4.985
2015 SCImago Journal Rankings: 3.549
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYang, ZFen_HK
dc.contributor.authorPoon, RTen_HK
dc.contributor.authorLuo, Yen_HK
dc.contributor.authorCheung, CKen_HK
dc.contributor.authorHo, DWen_HK
dc.contributor.authorLo, CMen_HK
dc.contributor.authorFan, STen_HK
dc.date.accessioned2008-06-12T06:39:57Z-
dc.date.available2008-06-12T06:39:57Z-
dc.date.issued2004en_HK
dc.identifier.citationJournal Of Immunology, 2004, v. 173 n. 4, p. 2507-2515en_HK
dc.identifier.issn0022-1767en_HK
dc.identifier.urihttp://hdl.handle.net/10722/49345-
dc.description.abstractThis study aims to investigate the potential role of vascular endothelial growth factor (VEGF) and VEGF-R2 (fetal liver kinase (Flk)-1) in mediating macrophage activities in small-for-size liver transplantation. A rat orthotopic liver transplantation model was performed using either whole, 50, or 30% liver grafts (both 50 and 30% were regarded as small-for-size) in syngeneic or allogeneic combinations, respectively. Firstly, the mRNA and protein levels of VEGF and Flk-1 in liver grafts were detected by RT-PCR and Western blot, and the number of Flk-1 + macrophages (labeled by ED1) was determined by flow cytometry. It was found that the small-for-size isografts and allografts presented higher levels of VEGF and Flk-1 expression than the whole isograft and allograft. In addition, a higher number of Flk-1 +ED1 + cells were detected in the small-for-size isografts and allografts than the whole isograft and allograft. Secondly, our study revealed that macrophage cell lines did not initially express detectable Flk-1, but could be induced by VEGF, and the inducible expression of Flk-1 in macrophages was related to their migration and proliferation activities. Finally, our study demonstrated that the induction of Flk-1 expression on macrophages by VEGF was associated with the expression of NF-κB and heat shock protein 90. In conclusion, the present study showed that the up-regulated expression of VEGF and its interaction with Flk-1 in small-for-size liver grafts might facilitate the activities of macrophages.en_HK
dc.format.extent420 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherAmerican Association of Immunologists. The Journal's web site is located at http://www.jimmunol.orgen_HK
dc.relation.ispartofJournal of Immunologyen_HK
dc.rightsThis is an author-produced version of a manuscript accepted for publication in The Journal of Immunology (The JI). The American Association of Immunologists, Inc. (The AAI), publisher of The JI, holds the copyright to this manuscript. This manuscript has not yet been copyedited or subjected to editorial proofreading by The JI; hence, it may differ from the final version published in The JI (online and in print). The AAI (The JI) is not liable for errors or omissions in this author-produced version of the manuscript or in any version derived from it by the National Institutes of Health or any other third party. The final, citable version of record can be found at www.jimmunol.orgen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshLiver Transplantation - immunologyen_HK
dc.subject.meshMacrophage Activation - immunologyen_HK
dc.subject.meshMacrophages - immunologyen_HK
dc.subject.meshVascular Endothelial Growth Factor A - biosynthesis - immunologyen_HK
dc.subject.meshVascular Endothelial Growth Factor Receptor-2 - biosynthesis - immunologyen_HK
dc.titleUp-regulation of vascular endothelial growth factor (VEGF) in small-for-size liver grafts enhances macrophage activities through VEGF receptor 2-dependent pathwayen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-1767&volume=173&issue=4&spage=2507&epage=2515&date=2004&atitle=Up-regulation+of+vascualr+endothelial+growth+factor+(VEGF)+in+small-for-size+liver+grafts+enhances+macrophage+activities+through+VEGF+receptor+2-dependent+pathwayen_HK
dc.identifier.emailPoon, RT: poontp@hkucc.hku.hken_HK
dc.identifier.emailLo, CM: chungmlo@hkucc.hku.hken_HK
dc.identifier.emailFan, ST: stfan@hku.hken_HK
dc.identifier.authorityPoon, RT=rp00446en_HK
dc.identifier.authorityLo, CM=rp00412en_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.pmid15294966en_HK
dc.identifier.scopuseid_2-s2.0-4043164854en_HK
dc.identifier.hkuros93952-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-4043164854&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume173en_HK
dc.identifier.issue4en_HK
dc.identifier.spage2507en_HK
dc.identifier.epage2515en_HK
dc.identifier.isiWOS:000223208900038-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridYang, ZF=14018809600en_HK
dc.identifier.scopusauthoridPoon, RT=7103097223en_HK
dc.identifier.scopusauthoridLuo, Y=37112607800en_HK
dc.identifier.scopusauthoridCheung, CK=8714367400en_HK
dc.identifier.scopusauthoridHo, DW=7402971906en_HK
dc.identifier.scopusauthoridLo, CM=7401771672en_HK
dc.identifier.scopusauthoridFan, ST=7402678224en_HK

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