Publications
Detailed Information
Hematein inhibits tumor necrotic factor-alpha-induced vascular cell adhesion molecule-1 and NF-kappa B-dependent gene expression in human vascular endothelial cells : Hematein inhibits tumor necrotic factor-α-induced vascular cell adhesion molecule-1 and NF-κB-dependent gene expression in human vascular endothelial cells
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Hong, JJ | - |
dc.contributor.author | Jeong, TS | - |
dc.contributor.author | Choi, JH | - |
dc.contributor.author | Park, JH | - |
dc.contributor.author | Lee, KY | - |
dc.contributor.author | Seo, YJ | - |
dc.contributor.author | Oh, SR | - |
dc.contributor.author | Oh, GT | - |
dc.date.accessioned | 2023-07-07T08:05:08Z | - |
dc.date.available | 2023-07-07T08:05:08Z | - |
dc.date.created | 2022-05-13 | - |
dc.date.issued | 2001-01 | - |
dc.identifier.citation | Biochemical and Biophysical Research Communications, Vol.281 No.5, pp.1127-1133 | - |
dc.identifier.issn | 0006-291X | - |
dc.identifier.uri | https://hdl.handle.net/10371/194900 | - |
dc.description.abstract | Monocyte adhesion to the endothelium via adhesion molecules is one of the earliest events in atherogenesis. It has been suggested that vascular cell adhesion molecule-1 (VCAM-1) plays a very important role in the recruitment of monocytes in atherosclerosis. The aim of our study was to evaluate whether hematein can influence the expression of VCAM-1 and the transcription of nuclear factor-kappaB (NF-kappaB)-dependent genes. Immunohistochemistry revealed that mouse aortic artery endothelial cells express VCAM-1 after feeding a high cholesterol diet for 8 weeks. Hematein dose dependently suppressed TNF-alpha induced VCAM-1 in both surface (30.8%) and soluble protein (65%) production in HUVECs. The transcription level of VCAM-1 was measured by Northern blot analysis, and decreased VCAM-1 protein expression was associated with a reduction of VCAM-1 mRNA expression. Transient transfection study of NF-kappaB promoter construct and electrophoretic mobility shift assay suggested that hematein inhibited both NF-kappaB-dependent gene expression and NF-kappaB activation induced by TNF-alpha. Our results suggest that the down-regulation of VCAM-1 expression by hematein may in part be due to the inhibition of NF-kappaB-dependent gene expression. (C) 2001 Academic Press. | - |
dc.language | 영어 | - |
dc.publisher | Academic Press | - |
dc.title | Hematein inhibits tumor necrotic factor-alpha-induced vascular cell adhesion molecule-1 and NF-kappa B-dependent gene expression in human vascular endothelial cells | - |
dc.title.alternative | Hematein inhibits tumor necrotic factor-α-induced vascular cell adhesion molecule-1 and NF-κB-dependent gene expression in human vascular endothelial cells | - |
dc.type | Article | - |
dc.identifier.doi | 10.1006/bbrc.2001.4480 | - |
dc.citation.journaltitle | Biochemical and Biophysical Research Communications | - |
dc.identifier.wosid | 000167642700011 | - |
dc.identifier.scopusid | 2-s2.0-0034809473 | - |
dc.citation.endpage | 1133 | - |
dc.citation.number | 5 | - |
dc.citation.startpage | 1127 | - |
dc.citation.volume | 281 | - |
dc.description.isOpenAccess | N | - |
dc.contributor.affiliatedAuthor | Park, JH | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.subject.keywordPlus | ATHEROSCLEROTIC LESIONS | - |
dc.subject.keywordPlus | SELECTIVE-INHIBITION | - |
dc.subject.keywordPlus | TRANSCRIPTION | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | VCAM-1 | - |
dc.subject.keywordPlus | SITES | - |
dc.subject.keywordPlus | MICE | - |
dc.subject.keywordPlus | SUBUNITS | - |
dc.subject.keywordPlus | BIOLOGY | - |
dc.subject.keywordPlus | DISEASE | - |
dc.subject.keywordAuthor | endothelial cells | - |
dc.subject.keywordAuthor | hematein | - |
dc.subject.keywordAuthor | vascular cell adhesion molecule | - |
- Appears in Collections:
- Files in This Item:
- There are no files associated with this item.
Item View & Download Count
Items in S-Space are protected by copyright, with all rights reserved, unless otherwise indicated.