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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-κB pathway

Title
Hepatocyte growth factor suppresses vascular endothelial growth factor-induced expression of endothelial ICAM-1 and VCAM-1 by inhibiting the nuclear factor-κB pathway
Authors
Min J.-K.Lee Y.-M.Jeong H.K.Kim Y.-M.Sung W.K.Lee S.-Y.Yong S.G.Goo T.O.Kwon Y.-G.
Ewha Authors
이수영오구택이영미
SCOPUS Author ID
이수영scopus; 오구택scopus; 이영미scopus
Issue Date
2005
Journal Title
Circulation Research
ISSN
0009-7330JCR Link
Citation
vol. 96, no. 3, pp. 300 - 307
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Vascular 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 IκB kinase activity, and this in turn prevented the activation of the inflammatory transcription factor NF-κB. Taken together, our results demonstrate that HGF suppresses VEGF-induced inflammation presumably by inhibiting the endothelial NF-κB 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.
DOI
10.1161/01.RES.0000155330.07887.EE
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자연과학대학 > 생명과학전공 > Journal papers
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