Cited 8 times in
Heparin Attenuates the Expression of TNFalpha-induced Cerebral Endothelial Cell Adhesion Molecule.
DC Field | Value | Language |
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dc.contributor.author | 김동구 | - |
dc.contributor.author | 김철훈 | - |
dc.contributor.author | 안영수 | - |
dc.contributor.author | 이정호 | - |
dc.date.accessioned | 2015-05-19T17:17:22Z | - |
dc.date.available | 2015-05-19T17:17:22Z | - |
dc.date.issued | 2008 | - |
dc.identifier.issn | 1226-4512 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/107863 | - |
dc.description.abstract | Heparin is a well-known anticoagulant widely used in various clinical settings. Interestingly, recent studies have indicated that heparin also has anti-inflammatory effects on neuroinflammation-related diseases, such as Alzheimer's disease and meningitis. However, the underlying mechanism of its actions remains unclear. In the present study, we examined the anti-inflammatory mechanism of heparin in cultured cerebral endothelial cells (CECs), and found that heparin inhibited the tumor necrosis factor alpha(TNFalpha)-induced and nuclear factor kappa B (NF-kappaB)-dependent expression of adhesion molecules, such as intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), which are crucial for inflammatory responses. Heparin selectively interfered with NF-kappaB DNA-binding activity in the nucleus, which is stimulated by TNFalpha. In addition, non-anticoagulant 2,3-O desulfated heparin (ODS) prevented NF-kappaB activation by TNFalpha, suggesting that the anti-inflammatory mechanism of heparin action in CECs lies in heparin's ability to inhibit the expression of cell adhesion molecules, as opposed to its anticoagulant actions. | - |
dc.description.statementOfResponsibility | open | - |
dc.format.extent | 231~236 | - |
dc.relation.isPartOf | KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.title | Heparin Attenuates the Expression of TNFalpha-induced Cerebral Endothelial Cell Adhesion Molecule. | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Pharmacology (약리학) | - |
dc.contributor.googleauthor | Jeong Ho Lee | - |
dc.contributor.googleauthor | Chul Hoon Kim | - |
dc.contributor.googleauthor | Gi Ho Seo | - |
dc.contributor.googleauthor | Jinu Lee | - |
dc.contributor.googleauthor | Joo Hee Kim | - |
dc.contributor.googleauthor | Dong Goo Kim | - |
dc.contributor.googleauthor | Young Soo Ahn | - |
dc.identifier.doi | 10.4196/kjpp.2008.12.5.231 | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A00396 | - |
dc.contributor.localId | A01057 | - |
dc.contributor.localId | A02246 | - |
dc.contributor.localId | A03130 | - |
dc.relation.journalcode | J02104 | - |
dc.identifier.eissn | 2093-3827 | - |
dc.identifier.pmid | 19967061 | - |
dc.subject.keyword | Anti-inflammation | - |
dc.subject.keyword | Cerebral endothelial cells | - |
dc.subject.keyword | Heparin | - |
dc.subject.keyword | ICAM-1 | - |
dc.subject.keyword | NF-κB | - |
dc.subject.keyword | VCAM-1 | - |
dc.contributor.alternativeName | Kim, Dong Goo | - |
dc.contributor.alternativeName | Kim, Chul Hoon | - |
dc.contributor.alternativeName | Ahn, Young Soo | - |
dc.contributor.alternativeName | Lee, Jeong Ho | - |
dc.contributor.affiliatedAuthor | Kim, Dong Goo | - |
dc.contributor.affiliatedAuthor | Kim, Chul Hoon | - |
dc.contributor.affiliatedAuthor | Ahn, Young Soo | - |
dc.contributor.affiliatedAuthor | Lee, Jeong Ho | - |
dc.rights.accessRights | free | - |
dc.citation.volume | 12 | - |
dc.citation.number | 5 | - |
dc.citation.startPage | 231 | - |
dc.citation.endPage | 236 | - |
dc.identifier.bibliographicCitation | KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY, Vol.12(5) : 231-236, 2008 | - |
dc.identifier.rimsid | 34736 | - |
dc.type.rims | ART | - |
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