Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 조인호 | * |
dc.contributor.author | 박정현 | * |
dc.date.accessioned | 2016-08-29T12:08:01Z | - |
dc.date.available | 2016-08-29T12:08:01Z | - |
dc.date.issued | 2016 | * |
dc.identifier.issn | 1537-1891 | * |
dc.identifier.other | OAK-16464 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/231076 | - |
dc.description.abstract | Uncontrolled hyperglycemia accelerates endothelial damage and vascular inflammation caused by proinflammatory cytokines including tumor necrosis factor α (TNFα), which leads to arteriosclerotic cardiovascular diseases such as myocardial infarction. Telmisartan, an angiotensin II type 1 receptor blocker (ARB), is prescribed for treatment of hypertensive patients with concurrent diabetes mellitus (DM). Although a few clinical trials have suggested that telmisartan decreases cardiovascular complications in diabetic patients, the molecular mechanism for the beneficial effects remains elusive. Here, we investigated a molecular mechanism and effects of telmisartan on the expression of vascular cell adhesion molecule-1 (VCAM-1) and attachment of monocytes onto endothelial cells induced by TNFα in hyperglycemia-treated bovine aortic endothelial cells (BAEC). Telmisartan dose-dependently decreased hyperglycemia-aggravated IκB kinase β (IKKβ) expression and nuclear factor-κB (NF-κB) p65-Ser536 phosphorylation, which accompanied a decrease in VCAM-1 expression and THP-1 monocytes adhesion. Among ARBs, including losartan and fimasartan, only telmisartan showed the inhibitory effects on expression of VCAM-1 and IKKβ, and phosphorylation of NF-κB p65-Ser536. The telmisartan's beneficial effects were not changed by pretreatment with GW9662, a specific and irreversible peroxisome proliferator-activated receptor γ (PPARγ) antagonist, although GW9662 clearly inhibited rosiglitazone-induced CD36 expression. Finally, ectopic expression of wild type (WT)-IKKβ significantly restored telmisartan-attenuated VCAM-1 expression, NF-κB p65-Ser536 phosphorylation, and THP-1 monocytes adhesion. Taken together, our findings demonstrate that telmisartan ameliorates hyperglycemia-exacerbated vascular inflammation, at least in part, by decreasing expression of IKKβ and VCAM-1 independently of PPARγ. Telmisartan may be useful for the treatment of DM-associated vascular inflammation and cardiovascular diseases. © 2015 Elsevier Inc. | * |
dc.language | English | * |
dc.publisher | Elsevier Inc. | * |
dc.subject | Fimasartan (PubChem CID: 9,870,652) | * |
dc.subject | Hyperglycemia | * |
dc.subject | IKKβ | * |
dc.subject | Losartan (PubChem CID: 3961) | * |
dc.subject | Telmisartan | * |
dc.subject | Telmisartan (PubChem CID: 65,999) | * |
dc.subject | Vascular inflammation | * |
dc.subject | VCAM-1 | * |
dc.title | Telmisartan attenuates hyperglycemia-exacerbated VCAM-1 expression and monocytes adhesion in TNFα-stimulated endothelial cells by inhibiting IKKβ expression | * |
dc.type | Article | * |
dc.relation.volume | 78 | * |
dc.relation.index | SCI | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 43 | * |
dc.relation.lastpage | 52 | * |
dc.relation.journaltitle | Vascular Pharmacology | * |
dc.identifier.doi | 10.1016/j.vph.2015.10.001 | * |
dc.identifier.wosid | WOS:000370114800006 | * |
dc.identifier.scopusid | 2-s2.0-84959112436 | * |
dc.author.google | Song K.-H. | * |
dc.author.google | Park J.-H. | * |
dc.author.google | Jo I. | * |
dc.author.google | Park J.-Y. | * |
dc.author.google | Seo J. | * |
dc.author.google | Kim S.A. | * |
dc.author.google | Cho D.-H. | * |
dc.contributor.scopusid | 조인호(26643129000;56663841900) | * |
dc.contributor.scopusid | 박정현(56937220800;57157650200;57157679600) | * |
dc.date.modifydate | 20240123112949 | * |