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Hepatocyte growth factor suppresses vascular endothelial growth factor-induced expression of endothelial ICAM-1 and VCAM-1 by inhibiting the nuclear factor-kappaB pathway

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dc.contributor.authorMin, Jeong-Ki-
dc.contributor.authorLee, Young-Mi-
dc.contributor.authorKim, Jeong Hun-
dc.contributor.authorKim, Young-Myeong-
dc.contributor.authorKim, Sung Wan-
dc.contributor.authorLee, Soo-Young-
dc.contributor.authorGho, Yong Song-
dc.contributor.authorOh, Goo Taeg-
dc.contributor.authorKwon, Young-Guen-
dc.date.accessioned2009-11-27T03:47:19Z-
dc.date.available2009-11-27T03:47:19Z-
dc.date.issued2005-01-08-
dc.identifier.citationCirc Res. 2005 Feb 18;96(3):300-7. Epub 2005 Jan 6.en
dc.identifier.issn1524-4571 (Electronic)-
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15637298-
dc.identifier.urihttps://hdl.handle.net/10371/16416-
dc.description.abstractVascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF) are potent angiogenic factors that have been used clinically to induce angiogenesis. However, concerns have been raised about VEGF because of its proinflammatory actions, which include enhancing the adhesion of leukocytes to endothelial cells. We have examined the possible antiinflammatory effects of HGF on the vasculature. HGF, unlike VEGF, did not alter leukocyte adhesion to endothelial cells. Instead it inhibited VEGF-induced leukocyte-endothelial cell interactions and the endothelial expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). In a skin inflammation model, VEGF-treated mice showed a significant increase of leukocytes infiltrated or adherent to the luminal surface of blood vessels, as compared with vehicle- or HGF-treated mice. The VEGF effect was markedly suppressed by coadministration of HGF. RT-PCR and promoter analysis revealed that HGF downregulated VEGF-mediated expression of ICAM-1 and VCAM-1 at the transcriptional level. Furthermore, these inhibitory effects coincided with suppression of IkappaB kinase activity, and this in turn prevented the activation of the inflammatory transcription factor NF-kappaB. Taken together, our results demonstrate that HGF suppresses VEGF-induced inflammation presumably by inhibiting the endothelial NF-kappaB pathway. This suggests that combined treatment with HGF and VEGF could be superior to treatment with either factor alone for enhancing therapeutic angiogenesis while avoiding inflammation.en
dc.language.isoenen
dc.publisherAmerican Heart Associationen
dc.subjectAnimalsen
dc.subjectCell Adhesion/physiologyen
dc.subjectCell Adhesion Molecules/biosynthesisen
dc.subjectCell Lineen
dc.subjectCell Line, Tumoren
dc.subjectChemotaxis, Leukocyte/physiologyen
dc.subjectEndothelial Cells/*metabolismen
dc.subjectEndothelium, Vascular/cytology/metabolismen
dc.subjectFemaleen
dc.subjectHepatocyte Growth Factor/*physiologyen
dc.subjectHumansen
dc.subjectI-kappa B Kinaseen
dc.subjectIntercellular Adhesion Molecule-1/*biosynthesisen
dc.subjectInterleukin-1/physiologyen
dc.subjectLeukocytes/metabolismen
dc.subjectMiceen
dc.subjectMice, Inbred Strainsen
dc.subjectNF-kappa B/*antagonists & inhibitors/*metabolismen
dc.subjectPhosphorylationen
dc.subjectProtein-Serine-Threonine Kinases/metabolismen
dc.subjectRNA, Messenger/antagonists & inhibitors/geneticsen
dc.subjectTranscription, Genetic/physiologyen
dc.subjectTranscriptional Activation/physiologyen
dc.subjectTumor Necrosis Factor-alpha/physiologyen
dc.subjectU937 Cells/chemistry/metabolismen
dc.subjectUmbilical Veins/cytologyen
dc.subjectVascular Cell Adhesion Molecule-1/*biosynthesisen
dc.subjectVascular Endothelial Growth Factors/*antagonists & inhibitors/*physiologyen
dc.titleHepatocyte growth factor suppresses vascular endothelial growth factor-induced expression of endothelial ICAM-1 and VCAM-1 by inhibiting the nuclear factor-kappaB pathwayen
dc.typeArticleen
dc.contributor.AlternativeAuthor민정기-
dc.contributor.AlternativeAuthor이영미-
dc.contributor.AlternativeAuthor김정훈-
dc.contributor.AlternativeAuthor김영명-
dc.contributor.AlternativeAuthor김성완-
dc.contributor.AlternativeAuthor이수영-
dc.contributor.AlternativeAuthor오구택-
dc.contributor.AlternativeAuthor권영근-
dc.identifier.doi10.1161/01.RES.0000155330.07887.EE-
Appears in Collections:
College of Medicine/School of Medicine (의과대학/대학원)Ophthalmology (안과학전공)Journal Papers (저널논문_안과학전공)
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