Clotting protein hinders nerve repair

A protein that helps keep a person from bleeding to death when cut or bruised also slows repair of nerve damage that results from injuries, according to a study with mice.

Wirelike nerve-cell extensions called axons run throughout the body. Most have a fatty sheath called myelin that acts as an insulator for the nerve’s electrical charges. When a nerve is damaged, the axon is exposed to blood and its constituents, including the clotting agent fibrin. A team reports in the March 14 Neuron that mice made to lack fibrin, by genetic engineering or the administration of drugs, recover much more quickly from a crush injury to a leg nerve than mice with a normal supply of the protein do.

In peripheral nerves–those extending beyond the brain and spinal cord–the myelin that coats axons is made by Schwann cells. Peripheral nerves can recover from injury only after a constellation of compounds induces these caretaker cells to make more myelin.

When nerves are damaged severely, however, fibrin comes into contact with Schwann cells and disrupts this process, says study coauthor Sidney Strickland, a neurobiologist at the Rockefeller University in New York. “As long as fibrin is around, the [Schwann] cells understand it’s an injury situation and that their main job is to proliferate,” he says. In so doing, they slough off their duties as myelin manufacturers, slowing nerve regrowth, he and his colleagues found.

In fact, examination of mouse tissue after these experiments showed roughly the same number of Schwann cells in the two groups of recovering mice. What differed, Strickland says, was the cells’ behavior. Those exposed to fibrin failed to produce myelin.

Peripheral axons do ultimately regrow as the fibrin becomes depleted, and after 28 days, mice in both groups showed about equal nerve recovery, Strickland says. The researchers suggest that although fibrin inhibits Schwann cells from making myelin, the protein might sometimes benefit nerve healing by giving axons enough time to reconnect with their associated muscles before new myelin sheaths enclose the axons.

“[Nerve] repair is a complex process, and no single mechanism will inhibit or enhance it,” says William Blakemore of Cambridge University in England.

Nevertheless, he says, “minimizing fibrin could be important.” Only further experiments on larger animals will show what impact fibrin inhibition might have on people, he says.

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