A Serine Protease Inhibitor To The Rescue

Plasminogen activators (PAs) are perhaps best known in the clinical world as intravascular clot busters. However, these fibrinolytic agents are also expressed in neurons and glia and have been implicated in axon outgrowth, regeneration, and neural injury. This week, Simonin et al. test the role of these serine proteases in axon degeneration in mice with progressive motor neuronopathy ( pmn/pmn). This so-called "dying back" motor neuron disease starts in axon terminals, followed by degeneration of cell bodies, and is paralleled by increases in PA levels in sciatic nerves. The pmn/pmn animals show weakness and muscle atrophy and die by 6 weeks of age. The authors crossed pmn mice with transgenic mice overexpressing neuroserpin, an axonally secreted inhibitor of PA. Surprisingly, the double-mutant mice lived 50% longer than their pmn/pmn counterparts. In addition to decreased PA activity, the double mutants had more myelinated axons and surviving motoneurons in the spinal cord and cranial nuclei.

Yannick Simonin, Yves Charron, Peter Sonderegger, Jean-Dominique Vassalli, and Ann C. Kato

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A Serine Protease Inhibitor To The Rescue