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The Journal of Neuroscience, October 1, 1999, 19(19):8244-8251

Knock-Out of the Neural Death Effector Domain Protein PEA-15 Demonstrates That Its Expression Protects Astrocytes from TNF-Induced Apoptosis

Daniel Kitsberg⁴, Etienne Formstecher¹, Mireille Fauquet¹, Miroslav Kubes^{1, 2}, Jocelyne Cordier¹, Brigitte Canton¹, GuoHua Pan³, Malvyne Rolli¹, Jacques Glowinski¹, and Hervé Chneiweiss¹

¹ Institut National de la Santé et de la Recherche Médicale U114, Chaire de Neuropharmacologie, Collège de France, 75231 Paris cedex 05, France ² Institute of Virology, Slovak Academy of Sciences, 842 46 Bratislava, Slovakia, ³ Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan 48109, and ⁴ Harvard Medical School, Boston, Massachusetts 02115

Apoptosis is a very general phenomenon, but only a few reports concern astrocytes. Indeed, astrocytes express receptors for tumor necrosis factor (TNF) , a cytokine demonstrated on many cells and tissues to mediate apoptosis after recruitment of adaptor proteins containing a death effector domain (DED). PEA-15 is a DED-containing protein prominently expressed in the CNS and particularly abundant in astrocytes. This led us to investigate if PEA-15 expression could be involved in astrocytic protection against deleterious effects of TNF. In vitro assays evidence that PEA-15 may bind to DED-containing protein FADD and caspase-8 known to be apical adaptors of the TNF apoptotic signaling. After generation of PEA-15 null mutant mice, our results demonstrate that PEA-15 expression increases astrocyte survival after exposure to TNF.

Key words: astrocytes; TNF; apoptosis; death effector domain; PEA-15; FADD; caspase

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Copyright © 1999 Society for Neuroscience  0270-6474/99/19198244-08$05.00/0

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