EMD Millipore eBook - 15

Analyzing Cell Death * Molecule that Destroys Apoptotic Cells also Repairs Damaged Axons

During programmed cell death, apoptotic
cells flag themselves for elimination by moving
a specific cell membrane component known as
phosphatidylserine (PS) from the inner membrane
to the cell surface, setting them up to be engulfed.
In contrast, broken axons in nerve cells send PSR-1
molecules an SOS alert. "The moment there is a
cut to the nerve cell we see a change in the cell
membrane PS composition, which acts as a
signal to PSR-1 molecules in the other part of
the nerve," said Dr. Xue.
"We propose that PS functions as a 'save-me'
signal for the distal fragment, allowing conserved
apoptotic cell clearance molecules to function in
re-establishing axonal integrity during regeneration
of the nervous system," wrote Dr. Xue and his
colleagues in the Nature paper.
One of the most encouraging finding is that
PSR-1 plays an early role in the axonal fusion
process required for neuroregeneration, he

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continued. "Whether human PSR has the capacity
to repair injured axons is still unknown," he said.
"But I think our new research findings will spur a
number of research groups to chase this question."
While biomedical researchers have had some
successes in repairing peripheral nerves and nerve
clusters outside the brain and spinal cord in
humans, there currently is no effective way to
regenerate broken nerve cells in the central
nervous system, noted Dr. Xue. Such nerve
damage can cause partial or total paralysis.
Xue, who first identified the PSR-1 receptor in
2003, said the collaboration between CU-Boulder
and UQ has pushed scientific discovery forward.
"We are trying to understand how PSR-1 removes
cells through apoptosis and necrosis, and they
are trying to understand if molecules involved in
apoptosis also play a role in the neuroregeneration
process," said Dr. Xue.
CU-Boulder postdoctoral researcher Yu-Zen

Chen, Ph.D., a Nature Communications paper
co-author, said the team currently is trying to find
ways to raise the level of the PSR-1 in nematode
cells, which likely would promote faster healing
in nerve axons. "We think the higher the PSR-1
level, the higher the repair capacity of the
molecule," said Dr. Chen.
According to Dr. Xue, C. elegans is an ideal
organism to use in the hunt for new therapeutics
to treat nerve damage because of its relatively
small, well-known genome and short life span
of just a few days. "This makes drug screening
much easier, faster and less expensive than using
a mouse model, for instance," he explained.
"The big finding is that we have a single
receptor that does two different jobs," noted
Dr. Xue. "We don't have a solution yet for treating
people with nerve damage, but we feel these
findings offer promise in seeking new and
effective therapeutics." n
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