As our bodies first form, developing cells are a lot like children put on the school bus with their names and addresses pinned to their shirts.
The notes identify one as a future heart cell, another as a liver cell, a third as a neuron. And that's what they each grow up to be.
But once those cells reach adulthood, changes to those original marching orders caused by aging, disease and other stressors like smoking can precipitate a kind of identity crisis, researchers at the University of Michigan Health System have found.
The cells start to forget things like which genes are supposed to be turned on and which turned off. This can lead to significant changes in their ability to function.
While microscopic, these changes can still have profound impacts on living beings. When this type of mutation was purposefully introduced into the heart muscle cells of mice, the normal functioning of the heart's electrical systems were disturbed, at times leading to dangerous arrhythmia, a new U-M study shows.
The results, published in the July issue of the Journal of Clinical Investigation, bring us one step closer to developing treatments for issues associated with aging or chronic diseases in which cells lose their ability to maintain a stable pattern of gene expression, says senior study author Gregory R. Dressler, Ph.D., collegiate professor of pathology research at the U-M Medical School.
"We're excited about this research because it suggests that these mutations can be the cause of disease as well as the result," says lead author Adam B. Stein, M.D., an assistant professor of cardiology at U-M.
Stein, Dressler and their colleagues are working in a relatively new area of research known as "epigenetics." It's well known that human beings pass a life code, bound up in the double helix of our DNA, from one generation to the next. What's less well understood is that they also transmit sets of instructions
|Contact: Ian Demsky|
University of Michigan Health System