- Oral presentation
- Open Access
Characterization of mice with a deletion of protein kinase G type I in cardiomyocytes and the effect on cardioprotection through either postconditioning or mitochondria-targeted S-nitrosothiol
© Methner et al; licensee BioMed Central Ltd. 2011
- Published: 1 August 2011
- Nitric Oxide
- Guanylyl Cyclase
- Ventricular Cardiomyocytes
- Ischemic Postconditioning
- Soluble Guanylyl Cyclase
Protein kinase G type I (PKGI/cGMP kinase I) plays a critical role in survival signalling of pre- and postconditioning. However, it is unclear whether cGKI exerts its protective effects in the cardiomyocyte or if other cardiac cell types are involved, and whether nitric oxide (NO) has cGKI-independent effects on cardiomyocytes mitochondria.
We developed mice with a cardiomyocyte-specific ablation of the cGKI gene (CMG-KO) and tested whether protection against reperfusion injury by ischemic postconditioning (IPost), soluble guanylyl cyclase (sGC) activation, the adenosine A2B receptor (A2BAR), or the mitochondria-targeted S-nitrosothiol (MitoSNO) was affected. MitoSNO accumulates within mitochondria, driven by the membrane potential, where it generates NO• and S-nitrosated thiol proteins .
While cardiomyocyte cGKI is important for the protection afforded via cGMP-signalling, beneficial effects of IPost, activation of the A2BAR, as well as direct NO effects via mitochondrial S-nitrosylation does not depend on cGKI in cardiomyocytes.
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