Stopping "Cellular Suicide" Could Boost Production In Biotech Labs

Every day, for reasons that are not clearly understood, some human cells commit suicide. Some cells, such as those that have been infected by a virus, kill themselves to preserve the health of the body as a whole. Other self-destruct simply because they sense that a threat to their survival or merely something unfamiliar is lurking nearby.

This process, called apoptosis or programmed cell death, is a normal biological occurrence that can promote proper organ development and help to prevent cancer. But it's unwelcome in modern biotech labs, where scientists turn living cells into miniature pharmaceutical factories that produce proteins, enzymes, antibodies and viruses to help patients with an array of illnesses. Apoptosis prompts many of these microscopic workers to put physiological "guns to their heads" after just a few days on the job. Working closely with molecular biologists, Johns Hopkins University engineer Michael J. Betenbaugh, is trying to disable these guns and allow the drug-making cells to lead longer, more productive lives.

"Ideally, we'd like to extend the lifetime of these cells and increase their efficiency in making biotech products that save people's lives," says Betenbaugh, an associate professor in the Department of Chemical Engineering.

His research has important implications. If scientists find a way to stop cellular suicide, they may be able to keep some cardiac cells from killing themselves after a heart attack. They may also be able to extend the life of artificial organs made from animal tissue.

The key is to halt apoptosis, which is often triggered by changes in a cell's environment. "It may be a viral infection, the loss of a key nutrient, radiation or a chemical toxin--all at sub-lethal levels," Betenbaugh explains. "These would not kill the cell by themselves. Nevertheless, the cell turns on this physiological chain of events that causes it to self-destruct."

In biotech labs, however, researchers want genetically-en

Contact: Phil Sneiderman
Johns Hopkins University

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