Enhancement of Nitric Oxide Production by Corticotropin-releasing Hormone (CRH) in Murine Microglial Cells, BV2
Immune Network
;
: 60-64, 2004.
Article
in Korean
| WPRIM
| ID: wpr-160482
ABSTRACT
BACKGROUND:
Microglial cells, major immune effector cells in the central nervous system, become activated in neurodegenerative disorders. Activated microglial cells produce proinflammatory mediators such as nitric oxide (NO), tumor necrosis factor-alpha and interleukin-1beta(IL-1beta). These proinflammatory mediators have been shown to be significantly increased in the neurodegenerative disorders such as Alzhimer's disease and Pakinson's disease. It was known that one of the neurodegeneration source is stress and it is important to elucidate mechanisms of the stress response for understanding the stress-related disorders and developing improved treatments. Because one of the neuropeptide which plays a main role in regulating the stress response is corticotropin- releasing hormone (CRH), we analyzed the regulation of NO release by CRH in BV2 murine microglial cell as macrophage in the brain.METHODS:
First, we tested the CRH receptor expression in the mRNA levels by RT-PCR. To test the regulation of NO release by CRH, cells were treated with CRH and then NO release was measured by Griess reagent assay.RESULTS:
Our study demonstrated that CRH receptor 1 was expressed in BV2 murine microglial cells and CRH treatment enhanced NO production. Furthermore, additive effects of lipopolysaccaride (LPS) and CRH were confirmed in NO production time dependantly.CONCLUSION:
Taken together, these data indicated that CRH is an important mediator to regulate NO release on microglial cells in the brain during stress.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Neuropeptides
/
Brain
/
RNA, Messenger
/
Corticotropin-Releasing Hormone
/
Central Nervous System
/
Tumor Necrosis Factor-alpha
/
Receptors, Corticotropin-Releasing Hormone
/
Neurodegenerative Diseases
/
Macrophages
/
Nitric Oxide
Language:
Korean
Journal:
Immune Network
Year:
2004
Type:
Article
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