Cited 18 times in
Heparin Inhibits NF-κB Activation and Increases Cell Death in Cerebral Endothelial Cells after Oxygen-Glucose Deprivation
DC Field | Value | Language |
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dc.contributor.author | 김철훈 | - |
dc.contributor.author | 안영수 | - |
dc.contributor.author | 이정호 | - |
dc.date.accessioned | 2014-12-21T16:51:32Z | - |
dc.date.available | 2014-12-21T16:51:32Z | - |
dc.date.issued | 2007 | - |
dc.identifier.issn | 0895-8696 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/96485 | - |
dc.description.abstract | Heparin is a classic anticoagulant that is commonly used in the treatment of acute ischemic stroke (AIS). Its use remains controversial, however, due to the risk of cerebral hemorrhagic transformation. In addition to anticoagulant effects, diverse effects on transcription factors can be caused by heparin. Among the transcription factors potentially affected is nuclear factor kappa B (NF-κB), a protein that is reportedly related to the survival of cerebral endothelial cells. We investigated the effect of heparin on NF-κB activation and cell death following oxygen-glucose deprivation (OGD), an experimental model of AIS. We subjected bEnd.3 cells from a murine cerebral microvascular endothelial cell line to OGD. We examined the effect of heparin on OGD-induced NF-κB activation and its mechanism of action, using electrophoretic mobility shift assays, reporter gene analysis, real-time RT-PCR, Western blot analysis, and confocal microscopy. We also measured the effect of heparin on OGD-induced cell death using an MTT assay. Heparin inhibited both tumor necrosis factor α- and OGD-induced NF-κB activation. Heparin was taken up by endocytosis and then entered the nucleus. Heparin did not affect the nuclear translocation of NF-κB, but instead inhibited the DNA binding of NF-κB in the nucleus. Cells were more susceptible to OGD-induced cell death after heparin treatment. Besides producing an anticoagulation effect, heparin also inhibits NF-κB activation, resulting in increased susceptibility to OGD-induced cell death. This effect may be responsible for hemorrhagic transformation in patients following heparin treatment for AIS. | - |
dc.description.statementOfResponsibility | open | - |
dc.format.extent | 145~154 | - |
dc.relation.isPartOf | JOURNAL OF MOLECULAR NEUROSCIENCE | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Animals | - |
dc.subject.MESH | Brain Neoplasms | - |
dc.subject.MESH | Cell Death/drug effects* | - |
dc.subject.MESH | Cell Line | - |
dc.subject.MESH | Cell Nucleus/drug effects | - |
dc.subject.MESH | Cell Nucleus/physiology | - |
dc.subject.MESH | Cerebrovascular Circulation/drug effects | - |
dc.subject.MESH | Cerebrovascular Circulation/physiology* | - |
dc.subject.MESH | Consensus Sequence | - |
dc.subject.MESH | Endothelium, Vascular/drug effects | - |
dc.subject.MESH | Endothelium, Vascular/physiology* | - |
dc.subject.MESH | Genes, Reporter | - |
dc.subject.MESH | Glucose/deficiency* | - |
dc.subject.MESH | Heparin/pharmacology* | - |
dc.subject.MESH | Hypoxia/physiopathology* | - |
dc.subject.MESH | Mice | - |
dc.subject.MESH | NF-kappa B/drug effects | - |
dc.subject.MESH | NF-kappa B/genetics | - |
dc.subject.MESH | NF-kappa B/physiology* | - |
dc.subject.MESH | Polymerase Chain Reaction | - |
dc.subject.MESH | Transfection | - |
dc.title | Heparin Inhibits NF-κB Activation and Increases Cell Death in Cerebral Endothelial Cells after Oxygen-Glucose Deprivation | - |
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 | Jinu Lee | - |
dc.contributor.googleauthor | Gi Ho Seo | - |
dc.contributor.googleauthor | Chul Hoon Kim | - |
dc.contributor.googleauthor | Young Soo Ahn | - |
dc.identifier.doi | 10.1007/s12031-007-0026-3 | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A01057 | - |
dc.contributor.localId | A02246 | - |
dc.contributor.localId | A03130 | - |
dc.relation.journalcode | J01609 | - |
dc.identifier.eissn | 1559-1166 | - |
dc.identifier.pmid | 17873298 | - |
dc.identifier.url | http://link.springer.com/article/10.1007/s12031-007-0026-3 | - |
dc.contributor.alternativeName | Kim, Chul Hoon | - |
dc.contributor.alternativeName | Ahn, Young Soo | - |
dc.contributor.alternativeName | Lee, Jeong Ho | - |
dc.contributor.affiliatedAuthor | Kim, Chul Hoon | - |
dc.contributor.affiliatedAuthor | Ahn, Young Soo | - |
dc.contributor.affiliatedAuthor | Lee, Jeong Ho | - |
dc.rights.accessRights | not free | - |
dc.citation.volume | 32 | - |
dc.citation.number | 2 | - |
dc.citation.startPage | 145 | - |
dc.citation.endPage | 154 | - |
dc.identifier.bibliographicCitation | JOURNAL OF MOLECULAR NEUROSCIENCE, Vol.32(2) : 145-154, 2007 | - |
dc.identifier.rimsid | 36107 | - |
dc.type.rims | ART | - |
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