Endothelial Cell Products as a Key Player in Hypoxia-Induced Nerve Cell Injury after Stroke
Journal of Korean Neurosurgical Society
; : 103-109, 2006.
Article
in English
| WPRIM (Western Pacific)
| ID: wpr-79528
Responsible library:
WPRO
ABSTRACT
OBJECTIVE:
Activated endothelial cells mediate the cascade of reactions in response to hypoxia for adaptation to the stress. It has been suggested that hypoxia, by itself, without reperfusion, can activate the endothelial cells and initiate complex responses. In this study, we investigated whether hypoxia-induced endothelial products alter the endothelial permeability and have a direct cytotoxic effect on nerve cells.METHODS:
Hypoxic condition of primary human umbilical vein endothelial cells(HUVEC) was induced by CoCl2 treatment in culture medium. Cell growth was evaluated by 3,4,5-dimethyl thiazole-3,5-diphenyl tetrazolium bromide (MTT) assay. Hypoxia-induced products (IL-1beta, TGF-beta1, IFN-gamma, TNF-alpha, IL-10, IL-6, IL-8, MCP-1 and VEGF) were assessed by enzyme-linked immunosorbent assay. Endothelial permeability was evaluated by Western blotting.RESULTS:
Prolonged hypoxia caused endothelial cells to secrete IL-6, IL-8, MCP-1 and VEGF. However, the levels of IL-1, IL-10, TNF-alpha, TGF-beta, IFN-gamma and nitric oxide remained unchanged over 48 h hypoxia. Hypoxic exposure to endothelial cells induced the time-dependent down regulation of the expression of cadherin and catenin protein. The conditioned medium taken from hypoxic HUVECs had the cytotoxic effect selectively on neuroblastoma cells, but not on astroglioma cells.CONCLUSION:
These results suggest the possibility that endothelial cell derived cytokines or other secreted products with the increased endothelial permeability might directly contribute to nerve cell injury followed by hypoxia.
Full text:
Available
Database:
WPRIM (Western Pacific)
Main subject:
Permeability
/
Astrocytoma
/
Umbilical Veins
/
Enzyme-Linked Immunosorbent Assay
/
Reperfusion
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Down-Regulation
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Blotting, Western
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Cytokines
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Interleukin-8
/
Transforming Growth Factor beta
Limits:
Humans
Language:
English
Journal:
Journal of Korean Neurosurgical Society
Year:
2006
Document type:
Article