Thierry Bordet, Henning Schmalbruch, Brigitte Pettmann, Albert Hagege, Laetitia Castelnau-Ptakhine, Axel Kahn, Georg Haase
J Clin Invest.
1999;
104(8):1077–1085
doi:10.1172/JCI6265
This article Copyright © 1999, The American Society for Clinical Investigation
Abstract
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ardiotrophin-1 (CT-1), an IL-6–related cytokine, causes hypertrophy of cardiac myocytes and has pleiotropic effects on various other cell types, including motoneurons. Here, we analyzed systemic CT-1 effects in progressive motor neuronopathy (pmn) mice that suffer from progressive motoneuronal degeneration, muscle paralysis, and premature death. Administration of an adenoviral CT-1 vector to newborn pmn mice leads to sustained CT-1 expression in the injected muscles and bloodstream, prolonged survival of animals, and improved motor functions. CT-1–treated pmn mice showed a significantly reduced degeneration of facial motoneuron cytons and phrenic nerve myelinated axons. The terminal innervation of skeletal muscle, grossly disturbed in untreated pmn mice, was almost completely preserved in CT-1–treated pmn mice. The remarkable neuroprotection conferred by CT-1 might become clinically relevant if CT-1 side effects, including cardiotoxicity, could be circumvented by a more targeted delivery of this cytokine to the nervous system.
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