Veksler said the team has been interested for many years in mechanisms of interaction between mitochondria and other organelles. They use "skinned cardiac fibers" whose outer membranes have been chemically removed which allows them to control the intracellular medium. They believed that in the tightly packed myocyte, that "mitochondria could push and compress nearby structures like myofibrils and modulate their functional properties."
This additional evidence of intracellular mechanical signaling "may have important physiological significance," Veksler said. He noted that a "number of studies indicate a sensitivity of nuclei to external mechanical forces and suggest that nuclear deformation could influence gene expression processes. Thus, we hypothesize that drugs or intracellular conditions inducing mitochrondrial swelling could by mechanical means influence gene expression.
"More studies are needed to explore this very intriguing and promising field of knowledge," he concluded.
In the experiment, the researchers found that in an artificial medium mimicking the cytosol, 10 micro-molar of valinomycin (a potassium ionophore that induces mitochondrial matrix swelling) decreased nuclear volume by a significant 12% ± 2%. And 150 micro-molar of diazoxide (a mitochondrial ATP-sensitive potassium channel opener) reduced nuclear volume a similar amount. "However, 150 micro-molar of 5-hydrooxydecanoate (thought to be a specific inhibitor of these channels), completely blocked the effect," according to the report, leading to the conclusion that: "mitochondria are able to induce nuclear deformation, suggesting that mitochondria may mechanically regulate nuclear function."
Veksler said one idea that needs to be checked out is: If this mechanical communication changes nuclear geometry, does it also impact nuclear functio
Source:American Physiological Society