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First direct mechanical communication of mitochondria, cardiomyocyte nucleus shown

In a paper being presented in two American Physiological Society sessions at Experimental Biology 2006, a joint Estonian-French team demonstrated "for the first time that mitochondria are able to induce nuclear deformation, suggesting that mitochondria may mechanically regulate nuclear function."

The team, which has been collaborating for over 10 years, reported that it recently "found a very interesting and unexpected phenomenon: various substances which increase mitochondrial size, also increased contractile force of cardiac fibers," or myofibrils. This effect isn't related to the mitochondrial energy production, they noted, and so a hypothesis was developed that "there might be in cardiac cells some form of mechanical signaling between organelles."

Vladimir Veksler, a former Soviet scientist who maintained his contacts with Estonian researchers after moving to Paris, said their latest research "shows that substances increasing the mitochondria can also compress the nuclear organelles, ensuring storage and treatment of genetic information."

Taken together, the results indicate that "the existence of such mechanical signaling between mitochondria and myofibrils opens a new possibility to search for drugs capable of increasing cardiac contractility," Veksler said.

*Presentations: The paper, "Direct mechanical communication between mitochondria and nucleus in cardiac cells," was chosen to be part of the "Physiological Genomics of Skeletal Muscle Adaptation in Health and Disease" Featured Topic session 199, sponsored by the APS Muscle Biology Group. Sunday April 2 at 10:30 a.m. in the Convention Center, Room 130, Moscone North. The paper will be presented at 11:15 a.m.

The research also will be presented 12:30-3 p.m. Monday April 3, APS Physiology Signaling in muscle session 486.6/board #C732. Research was performed by Allen Kaasik, Department of Pharmacology, University of Tartu, Estonia, who collaborates with Renée Ventura-Cla
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Source:American Physiological Society


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