Key result
Diazoxide, a selective MitoKATP channel activator, caused significant translocation of PKCε to myofibrillar-like structures in cultured adult rat ventricular myocytes, possibly via ROS production.
Why the study?
Does diazoxide induce PKCε translocation in adult rat ventricular myocytes?
Does diazoxide induce PKCε translocation in adult rat ventricular myocytes?
Opening of MitoKATP channels with diazoxide activates and translocates PKCε in rat ventricular myocytes, likely downstream via ROS production.
Hypothesis-generating for MitoKATP-PKCε signaling in rodent myocytes; leaves open translation to human cardioprotection.
This study aimed to investigate the effects of mitochondrial ATP-sensitive potassium (MitoKATP) channel opening on the translocation of protein kinase C epsilon (PKCε). In addition, we aimed to determine the relationship between PKCε translocation and the production of reactive oxygen species (ROS). PKCε protein expression in cultured adult rat ventricular myocytes was investigated by immunofluorescence and Western blotting. Diazoxide (DZ), a selective MitoKATP channel activator, caused a significant translocation to myofibrillar-like structures in cultured adult rat ventricular myocytes. N-2-Mercaptopropionylglycine, a free radical scavenger, could partially inhibit the translocation of PKCε induced by DZ. By contrast, chelerythrine, a selective PKC inhibitor, could completely block the translocation of PKCε induced by DZ. The opening of MitoKATP channels might activate and cause PKCε to translocate into myofibrillar-like structures. PKCε activation occurred downstream of the MitoKATP channel, possibly as a result of ROS production that occurred after the MitoKATP channels opened.
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Li et al. (2014) studied this question. Diazoxide was evaluated on Translocation of protein kinase C epsilon (PKCε). Diazoxide, a selective MitoKATP channel activator, caused significant translocation of PKCε to myofibrillar-like structures in cultured adult rat ventricular myocytes, possibly via ROS production.
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