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The Journal of Neuroscience, May 15, 1999, 19(10):3809-3817
CD95 Ligand (Fas-L/APO-1L) and Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand Mediate Ischemia-Induced Apoptosis in Neurons
Ana Martin-Villalba1, Ingrid Herr3, Irmela Jeremias3, Michael Hahne5, Roland Brandt2, Johannes Vogel1, Johannes Schenkel1, Thomas Herdegen4, and Klaus-Michael Debatin3 Departments of 1 Physiology and 2 Neurobiology, University of Heidelberg, D-69120 Heidelberg, Germany, 3 Division of Molecular Oncology, Deutsches Krebsforschungszentrum, D-69120 Heidelberg, Germany, 4 Department of Pharmacology, University of Kiel, D-24118 Kiel, Germany, and 5 Department of Biochemistry, University of Lausanne, CH-1000 Lausanne, Switzerland
Programmed cell death plays an important role in the neuronal degeneration after cerebral ischemia, but the underlying mechanisms are not fully understood. Here we examined, in vivo and in vitro, whether ischemia-induced neuronal death involves death-inducing ligand/receptor systems such as CD95 and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). After reversible middle cerebral artery occlusion in adult rats, both CD95 ligand and TRAIL were expressed in the apoptotic areas of the postischemic brain. Further recombinant CD95 ligand and TRAIL proteins induced apoptosis in primary neurons and neuron-like cells in vitro. The immunosuppressant FK506, which most effectively protects against ischemic neurodegeneration, prevented postischemic expression of these death-inducing ligands both in vivo and in vitro. FK506 also abolished phosphorylation, but not expression, of the c-Jun transcription factor involved in the transcriptional control of CD95 ligand. Most importantly, in lpr mice expressing dysfunctional CD95, reversible middle cerebral artery occlusion resulted in infarct volumes significantly smaller than those found in wild-type animals. These results suggest an involvement of CD95 ligand and TRAIL in the pathophysiology of postischemic neurodegeneration and offer alternative strategies for the treatment of cardiovascular brain disease.
Key words: CD95 ligand; TRAIL; apoptosis; focal ischemia; neurons; lpr mouse
Copyright © 1999 Society for Neuroscience 0270-6474/99/19103809-09$05.00/0
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