The Roles of SEK1 in Nitric Oxide (NO) Induced Apoptsis of RAW264.7 cells.
- Author:
Jeong Ho LEE
;
Hong Seob SO
;
Byung Hak JUNG
- Publication Type:Original Article
- Keywords:
Nitric oxide (NQ);
Apoptosis;
SEK1
- MeSH:
Apoptosis;
Caspase 3;
Cell Death;
Cell Survival;
Clone Cells;
Macrophages;
Mortality;
Nitric Oxide*;
Nitroprusside;
Phosphotransferases;
Protein Kinases
- From:Korean Journal of Immunology
1999;21(1):55-61
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Nitric oxide (NO) induces apoptotic cell death in murine RAW 264.7 macrophages. To elucidate the roles of SEK1/MKK4, a upstream kinase for both c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) and p38 kinase, on NO-induced apoptosis, we generated clones of RAW 264.7 cells which stably overexpressd kinase inactive SEK1 (RAW/SEK1-Kl) or wild type SEK1 (RAW/SEK1-WT). Treatment of kinase inactive SEK1 transfected RAW 264.7 cells (RAW/SEK1-Kl) with sodium nitroprusside (SNP), a NO generating agent, significantly decreased the cell viability up to 20% of RAW control cells which were treated with the same amount of SNP. However, RAW/SEK1-WT cells were less susceptible to NO induced apoptosis. For a while, caspase-3 like activity in NO treated RAW/SEK1-Kl cells was significantly increased with parallell to apoptotic death rate. However, caspase1 like activity was not affected by NO in any transfectants. The NO induced apoptosis in RAW/SEK1-Kl cells was significantly prevented by the addition of caspase-3 like inhibitor (N-Ac- DEVD-CHO). In addition, the phosphotransferase activity of JNK1 in NO-treated RAW/SEK1-WT is significantly increased, but not in RAW/SEK1-Kl cells. These results suggest that SEK1 may play anti-apoptotic role in RAW cells from NO-induced apoptosis.
