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Catalase protects cardiomyocytes via its inhibition of nitric oxide synthesis
Han-Jung Chae1, Ki-Chan Ha, Do-Sung Kim
1Department of Dental Pharmacology and Wonkwang Biomaterial Implant Research Institute, School of Dentistry, Wonkwang University, Chonbuk 570-749, Republic of Korea.
Abstract:
Nitric oxide (NO) has been reported to play an important role as an effector molecule in cytokine signal transduction in cardiomyocytes. A treatment of neonatal rat ventricular cardiomyocytes with interleukin-1 beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha), and interferon-gamma (IFN-gamma) induces apoptosis via an NO-dependent pathway. However, cardiomyocytes were more resistant to NO-dependent cell death in the presence of catalase, while producing inducible nitric oxide synthase. This paper reports that catalase stimulates the NF-kappaB-binding affinity. However, the NO synthase activity is abolished by the addition of catalase, suggesting that H(2)O(2) is involved in NO synthesis in a posttranslation state. The catalase-induced inhibition of NO was partially but significantly reversed by H(4)B, an important cofactor of NO synthesis. Treatment of myocytes with IL-1beta, TNF-alpha, and IFN-gamma induced a significant increase in the formation of peroxynitrite, and a pretreatment with catalase was found to quench the production of peroxynitrite. This paper shows that the catalase activity was significantly down-regulated by H(4)B in a concentration-dependent manner. The treatment of H(4)B induced reactive oxygen species (ROS) release in cardiac cell system. These results suggest that catalase interferes with NO and peroxynitrite production as well as with the related apoptosis of cardiomyocytes. This study also shows that the catalase-induced inhibition of NO release may be reversed by H(4)B by the release of ROS.
Insights
Catalase inhibits nitric oxide (NO) and peroxynitrite production, protecting cardiomyocytes from cytokine-induced apoptosis. Tetrahydrobiopterin (H4B) reverses this inhibition by releasing reactive oxygen species (ROS).
Area of Science:
- Cardiovascular Biology
- Biochemistry
- Cellular Signaling
Background:
- Nitric oxide (NO) mediates cytokine signaling and apoptosis in cardiomyocytes.
- Cytokines like IL-1beta, TNF-alpha, and IFN-gamma induce NO-dependent apoptosis.
- Catalase confers resistance to NO-dependent cell death in cardiomyocytes.
Purpose of the Study:
- To investigate the role of catalase in NO synthesis and cardiomyocyte apoptosis.
- To elucidate the interaction between catalase, hydrogen peroxide (H2O2), and NO production.
- To determine the effect of tetrahydrobiopterin (H4B) on NO and reactive oxygen species (ROS) in this system.
Main Methods:
- Treatment of neonatal rat ventricular cardiomyocytes with cytokines (IL-1beta, TNF-alpha, IFN-gamma).
- Assessment of NO production, inducible nitric oxide synthase (iNOS) activity, and peroxynitrite formation.
- Enzyme assays for catalase activity and NF-kappaB binding affinity.
- Investigation of H4B and H2O2 effects on NO synthesis and ROS release.
Main Results:
- Catalase abolished NO synthase activity, suggesting H2O2 involvement in post-translational NO regulation.
- Catalase inhibited peroxynitrite formation induced by cytokines.
- H4B partially reversed catalase-induced NO inhibition and induced ROS release.
- H4B down-regulated catalase activity in a concentration-dependent manner.
Conclusions:
- Catalase interferes with NO and peroxynitrite production, impacting cardiomyocyte apoptosis.
- H4B can reverse catalase-mediated inhibition of NO release through ROS generation.
- These findings highlight a complex interplay between ROS, NO, and apoptosis regulation in cardiomyocytes.
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