I am working in collaboration with a postdoc in the lab (Bahador Marzban) to develop a device designed to work in concert with our respirometer that will support simultaneous measurements of mitochondrial oxygen consumption rates and fluorescently labelled biochemical species including pH, [K+], and membrane potential. With this device and/or by available alternative approaches, I will integrate the information from fluorometric and respirometry analyses to determine whether mitochondrial K+ transport processes affect bioenergetics via pH regulation, under different respiratory states, which will augment computational models for mitochondrial energetics to account for K+transport and pH regulation.
- Mitochondrial K+ channels, such as the molecularly characterized ATP-sensitive K+ channel (mitoKATP) constitute targets for preconditioning with pharmacological activators conferring protection against ischemia-reperfusion injury
- The ATP inhibition constant for mitoKATP is in the micromolar range, well below that of physiological concentrations in tissues, such as the brain and heart, suggesting that the channel is always closed
- Studies assessing metabolic function in HeLa cells indicate that knockout of mitoKatp affects metabolic function, supporting a potential physiological function
Do mitochondrial K+ transport processes regulate bioenergetics via pH control under physiological conditions?
