Heparin inhibits NF-kappaB activation and increases cell death in cerebral endothelial cells after oxygen-glucose deprivation.

Heparin inhibits NF-kappaB activation and increases cell death in cerebral endothelial cells after oxygen-glucose deprivation. Research Abstract Details 

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Heparin inhibits NF-kappaB activation and increases cell death in cerebral endothelial cells after oxygen-glucose deprivation. Abstract Text:

Jeong Ho Lee,Jinu Lee,Gi Ho Seo,Chul Hoon Kim,Young Soo Ahn,Jeong Ho Lee,Jinu Lee,Gi Ho Seo,Chul Hoon Kim,Young Soo Ahn,

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-kappaB), a protein that is reportedly related to the survival of cerebral endothelial cells. We investigated the effect of heparin on NF-kappaB 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-kappaB 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 alpha- and OGD-induced NF-kappaB activation. Heparin was taken up by endocytosis and then entered the nucleus. Heparin did not affect the nuclear translocation of NF-kappaB, but instead inhibited the DNA binding of NF-kappaB in the nucleus. Cells were more susceptible to OGD-induced cell death after heparin treatment. Besides producing an anticoagulation effect, heparin also inhibits NF-kappaB 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.

Heparin inhibits NF-kappaB activation and increases cell death in cerebral endothelial cells after oxygen-glucose deprivation. Publishing Authors By Initials

JH Lee,J Lee,GH Seo,CH Kim,YS Ahn,JH Lee,J Lee,GH Seo,CH Kim,YS Ahn,

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Heparin inhibits NF-kappaB activation and increases cell death in cerebral endothelial cells after oxygen-glucose deprivation. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Journal of molecular neuroscience : MN

VOLUME: 32

Page Numbers: 145-54

Journal Abbreviation: J. Mol. Neurosci.

ISSN: 0895-8696

DAY: 17

MONTH: 09

YEAR: 2007

Heparin inhibits NF-kappaB activation and increases cell death in cerebral endothelial cells after oxygen-glucose deprivation. Information

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LANGUAGE: eng

NlmUniqueID: 9002991

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AFFILIATION: Department of Pharmacology, Yonsei University College of Medicine, Seoul, South Korea.

Country: United States

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MEDLINETA: J Mol Neurosci

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