Aaron DiAntonio and colleagues identify protein required to regrow injured nerves in limbs

DLK promotes axonal response following injury Read More

From the WUSTL Newsroom

A protein required to regrow injured peripheral nerves has been identified by researchers at Washington University School of Medicine in St. Louis.

The finding, in mice, has implications for improving recovery after nerve injury in the extremities. It also opens new avenues of investigation toward triggering nerve regeneration in the central nervous system, notorious for its inability to heal.

Peripheral nerves provide the sense of touch and drive the muscles that move arms and legs, hands and feet. Unlike nerves of the central nervous system, peripheral nerves can regenerate after they are cut or crushed. But the mechanisms behind the regeneration are not well understood.

In the new study, published online June 20 in Neuron, the scientists show that a protein called dual leucine zipper kinase (DLK) regulates signals that tell the nerve cell it has been injured – often communicating over distances of several feet. The protein governs whether the neuron turns on its regeneration program.

“DLK is a key molecule linking an injury to the nerve’s response to that injury, allowing the nerve to regenerate,” says Aaron DiAntonio, MD, PhD, professor of developmental biology. “How does an injured nerve know that it is injured? How does it take that information and turn on a regenerative program and regrow connections? And why does only the peripheral nervous system respond this way, while the central nervous system does not? We think DLK is part of the answer.”

In addition, it was shown many years ago that axons regrow faster after a second injury than axons injured only once. In other words, injury itself increases an axon’s ability to regenerate. Furthering this work, first author Jung Eun Shin, graduate research assistant, and her colleagues found that DLK is required to promote this accelerated growth.

“A neuron that has seen a previous injury now has a different regenerative program than one that has never been damaged,” Shin says. “We hope to be able to identify what is different between these two neurons — specifically what factors lead to the improved regeneration after a second injury. We have found that activated DLK is one such factor. We would like to activate DLK in a newly injured neuron to see if it has improved regeneration.”

For more from Julia Evangelou Strait of the WUSTL Newsroom, click here.

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Posted on June 21, 2012
Posted in: Axon Injury & Repair, News Authors: , ,