Korean J Anat.  1999 Oct;32(5):709-716.

The Role of Sek1 in Protecting NO-induced Apoptosis in H9c2 cells by Inhibiting Caspase 3 Activation

• Oh J
• Park R
• So HS
• Moon YJ
• Baeck Y
• Choi MK
• Park OK
• Lee HI
• Chung YT

Abstract

The stress activated protein kinase, or Jun N-terminal kinase (SAPKs/JNKs), is activated in response to a variety of cellular stresses such as changes in osmolarity and metabolism, DNA damage, heat shock, ischemia, and inflammatory cytokines. Sek1 (JNKK/MKK4) is a direct activator of SAPKs/JNKs in response to environmental stresses or mitogenic factors. Thus, this study was conducted to investigate the role of Sek1 on nitric oxide (NO) induced apoptotic signaling pathway in H9c2 cell. The viability of SNP (Sodium Nitroprusside) treated inactive Sek1 kinase transfectants [Sek1/KI H9c2] is significantly decreased and SNP induce DNA fragmentation in Sek1/KI H9c2. Interestingly, concomitantly with SNP induced injuries, caspase 3-like activity is increased but caspase 1 like activity is not changed in Sek1/KI H9c2. Whereas wild type Sek1 kinase transfectants [Sek1/WT H9c2] is less susceptible to SNP induced apoptosis. In Sek1/KI H9c2, the injuries and DNA fragmentation by SNP is protected by adding Ac-DEVD-AMC, caspase 3 inhibitor. In conclusion, these results suggest that Sek1 plays a role in protecting NO-induced apoptosis and DNA fragmentaion in H9c2 cells by inhibiting caspase 3-like activation.

Keyword

Stress activated protein kinase; Nitric oxide; Apoptosis; Sek1; Caspase

MeSH Terms

Apoptosis*
Caspase 1
Caspase 3*
Cytokines
DNA
DNA Damage
DNA Fragmentation
Hot Temperature
Ischemia
Metabolism
Nitric Oxide
Osmolar Concentration
Phosphotransferases
Protein Kinases
Shock
Caspase 1
Caspase 3
Cytokines
DNA
Nitric Oxide
Phosphotransferases
Protein Kinases