A mix of serendipity and dogged laboratory work allowed a diverse team of University of Pittsburgh scientists to report in the Oct. 1 issue of Nature Cell Biology that they had solved the mystery of a basic biological function essential to cellular health.
By discovering a mechanism by which mitochondria tiny structures inside cells often described as "power plants" signal that they are damaged and need to be eliminated, the Pitt team has opened the door to potential research into cures for disorders such as Parkinson's disease that are believed to be caused by dysfunctional mitochondria in neurons.
"It's a survival process. Cells activate to get rid of bad mitochondria and consolidate good mitochondria. If this process succeeds, then the good ones can proliferate and the cells thrive," said Valerian Kagan, Ph.D., D.Sc., a senior author on the paper and professor and vice chair of the Pitt Graduate School of Public Health's Department of Environmental and Occupational Health. "It's a beautiful, efficient mechanism that we will seek to target and model in developing new drugs and treatments."
Dr. Kagan, who, as a recipient of a Fulbright Scholar grant, currently is serving as visiting research chair in science and the environment at McMaster University in Ontario, Canada, likened the process to cooking a Thanksgiving turkey.
"You put the turkey in the oven and the outside becomes golden, but you can't just look at it to know it's ready. So you put a thermometer in, and when it pops up, you know you can eat it," he said. "Mitochondria give out a similar 'eat me' signal to cells when they are done functioning properly."
Cardiolipins, named because they were first found in heart tissue, are a component on the inner membrane of mitochondria. When a mitochondrion is damaged, the cardiolipins move from its inner membrane to its outer membrane, where they encourage the cell to destroy the entire mitochondrion.
|Contact: Allison Hydzik|
University of Pittsburgh Schools of the Health Sciences