The Role of Sek1 in Protecting NO-induced Apoptosis in H9c2 cells by Inhibiting Caspase 3 Activation.
- Author:
Jaymin OH
1
;
Raekil PARK
;
Hong Seob SO
;
Yeon Ja MOON
;
Yonga BAECK
;
Min Kyu CHOI
;
Ock Kyu PARK
;
Ho Ik LEE
;
Yeun Tai CHUNG
Author Information
1. Department of Anatomy, School of Medicine, Wonkwang University, Iksan, Korea.
- Publication Type:Original Article
- Keywords:
Stress activated protein kinase;
Nitric oxide;
Apoptosis;
Sek1;
Caspase
- MeSH:
Apoptosis*;
Caspase 1;
Caspase 3*;
Cytokines;
DNA;
DNA Damage;
DNA Fragmentation;
Hot Temperature;
Ischemia;
Metabolism;
Nitric Oxide;
Osmolar Concentration;
Phosphotransferases;
Protein Kinases;
Shock
- From:Korean Journal of Anatomy
1999;32(5):709-716
- CountryRepublic of Korea
- Language:Korean
-
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.
