Korean J Immunol.  1999 Mar;21(1):55-61.

The Roles of SEK1 in Nitric Oxide (NO) Induced Apoptsis of RAW264.7 cells


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.


Nitric oxide (NQ); Apoptosis; SEK1
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