Programmed Cell Death: Aging Body Produces Small Amount Of Proteins
Researchers at the University of Missouri-Columbia have identified how the kidney cells' self-destruct messages are spread by finding what may lead to improved kidney function in the elderly.
As individuals age, organs such as the kidneys become increasingly susceptible to injury, along with a lowered ability to self-repair. For this study, researchers discovered how a cellular signal that causes kidney cells to die can make kidneys more prone to injury.
During the study, they zeroed in on how aging individuals have a reduced ability to produce a protein known as alpha (E)-catenin. These proteins typically serve a number of functions in the cell, including maintaining the cell's shape and structure. They also regulate how quickly the cells multiply.
Yet the protein is lost when cells grow more quickly, resulting in an increased production of kidney cells. From there, a signal in the cell is then activated for these extra cells to be destroyed, causing unregulated apoptosis--otherwise known as programmed cell death--with too many of these cells self-destructing and kidney function being compromised.
"Apoptosis is vital to the health of organs, because it kills cells that are no longer needed or that pose a threat to the organism," Alan Parrish, Ph.D., associate professor of medical pharmacology and physiology at the MU School of Medicine and co-author of the study, said in a news release. "But when this self-destruct sequence is activated due to a lack of alpha (E)-catenin, healthy cells end up being destroyed. We don't know why the aging body doesn't produce enough of this protein. However, we've found how this self-destruct message is being communicated."
Yet by better identifying this self-destruction, researchers are hopeful that they could understand and ultimately improve the health and function of this vital organ.
"Now that we have identified this communication pathway, how do we manipulate this pathway to protect the kidney?" Parrish said. "We know that as we age we're losing alpha (E)-catenin, so we hope to find out how we can either prevent that loss or substitute for its function. That's what we will study next."
More information regarding the findings can be seen via the journal Apoptosis.
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