c‐Jun Contributes to Amyloid β‐Induced Neuronal Apoptosis but Is Not Necessary for Amyloid β‐Induced c‐jun Induction

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Abstract
: The role of gene expression in neuronal apoptosis may be cell- and apoptotic stimulus-specific. Previously, we and others showed that amyloid β (Aβ)-induced neuronal apoptosis is accompanied by c-jun induction. Moreover, c-Jun contributes to neuronal death in several apoptosis paradigms involving survival factor withdrawal. To evaluate the role of c-Jun in Aβ toxicity, we compared Aβ-induced apoptosis in neurons from murine fetal littermates that were deficient or wild-type with respect to c-Jun. We report that neurons deficient for c-jun are relatively resistant to Aβ toxicity, suggesting that c-Jun contributes to apoptosis in this model. When changes in gene expression were quantified in neurons treated in parallel, we found that Aβ treatment surprisingly led to an apparent activation of the c-jun promoter in both c-jun-deficient and wild-type neurons, suggesting that c-Jun is not necessary for activation of the c-jun promoter. Indeed, several genes induced by Aβ in wild-type neurons were also induced in c-jun-deficient neurons, including c-fos, fosB, ngfi-B, and iκB. In summary, these results indicate that c-Jun contributes to Aβ-induced neuronal death but that c-Jun is not necessary for c-jun induction.