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The Journal of Neuroscience, November 1, 2001, 21(21):8572-8585

Transforming Growth Factor  (TGF) Mediates Schwann Cell Death In Vitro and In Vivo: Examination of c-Jun Activation, Interactions with Survival Signals, and the Relationship of TGF-Mediated Death to Schwann Cell Differentiation

David B. Parkinson¹, Ziping Dong⁴, Howard Bunting¹, Jonathan Whitfield³, Carola Meier⁵, Hélène Marie², Rhona Mirsky¹, and Kristjan R. Jessen¹

¹ Departments of Anatomy and Developmental Biology and ² Physiology, and ³ Eisai London Research, University College London, London WC1E 6BT, United Kingdom, ⁴ Reneuron Ltd., Denmark Hill, London SE5 8AF, United Kingdom, and ⁵ Institut für Neuroanatomie, Med. Einrichtungen der Ruhr-Universität, 44780 Bochum, Germany

In some situations, cell death in the nervous system is controlled by an interplay between survival factors and negative survival signals that actively induce apoptosis. The present work indicates that the survival of Schwann cells is regulated by such a dual mechanism involving the negative survival signal transforming growth factor  (TGF), a family of growth factors that is present in the Schwann cells themselves. We analyze the interactions between this putative autocrine death signal and previously defined paracrine and autocrine survival signals and show that expression of a dominant negative c-Jun inhibits TGF-induced apoptosis. This and other findings pinpoint activation of c-Jun as a key downstream event in TGF-induced Schwann cell death. The ability of TGF to kill Schwann cells, like normal Schwann cell death in vivo, is under a strong developmental regulation, and we show that the decreasing ability of TGF to kill older cells is attributable to a decreasing ability of TGF to phosphorylate c-Jun in more differentiated cells.

Key words: autocrine signals; apoptosis; nerve development; peripheral nerve; nerve injury; nerve regeneration

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Copyright © 2001 Society for Neuroscience  0270-6474/01/21218572-14$05.00/0

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