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Differential Induction of Immediate Early Gene Proteins in Cultured Neurons by β‐Amyloid (Aβ): Association of c‐Jun with Aβ‐Induced Apoptosis

Differential Induction of Immediate Early Gene Proteins in Cultured Neurons by β‐Amyloid (Aβ):... Abstract: β‐Amyloid (Aβ) is a 39–42 amino acid that is the primary component of plaques in Alzheimer's disease (AD). Previous studies from our laboratory and others have shown that Aβ induces neurodegeneration via apoptosis in vitro, suggesting that Aβ may also initiate an apoptotic pathway of cell death in AD. Apoptosis has been suggested to proceed by a gene‐directed program in several systems. Accordingly, we have investigated whether Aβ‐mediated apoptosis is associated with the induction of genes that may regulate or play a role in cell death in vitro. Immediate early genes (IEGs) respond to cellular stimuli and participate in cellular signaling pathways. The protein products of some IEGs, e.g., c‐jun, are capable of forming dimers and acting as transcriptional regulatory proteins, and have been implicated in apoptosis in both nonneuronal and neuronal cells. In this study, we report a selective and abnormally sustained induction of c‐Jun in cultured hippocampal neurons treated with Aβ. In addition, we describe the lack of induction of c‐Jun in neurons that are relatively resistant to Aβ‐mediated toxicity, and a correspondence between immunoreactivity for c‐Jun and changes in nuclear morphology that are indicative of apoptosis. These data demonstrate that c‐Jun is induced in cultured neurons that undergo Aβ‐mediated apoptosis and suggest that c‐Jun may participate in a cell death program in these neurons. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Neurochemistry Wiley

Differential Induction of Immediate Early Gene Proteins in Cultured Neurons by β‐Amyloid (Aβ): Association of c‐Jun with Aβ‐Induced Apoptosis

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References (70)

Publisher
Wiley
Copyright
Copyright © 1995 Wiley Subscription Services
ISSN
0022-3042
eISSN
1471-4159
DOI
10.1046/j.1471-4159.1995.65041487.x
Publisher site
See Article on Publisher Site

Abstract

Abstract: β‐Amyloid (Aβ) is a 39–42 amino acid that is the primary component of plaques in Alzheimer's disease (AD). Previous studies from our laboratory and others have shown that Aβ induces neurodegeneration via apoptosis in vitro, suggesting that Aβ may also initiate an apoptotic pathway of cell death in AD. Apoptosis has been suggested to proceed by a gene‐directed program in several systems. Accordingly, we have investigated whether Aβ‐mediated apoptosis is associated with the induction of genes that may regulate or play a role in cell death in vitro. Immediate early genes (IEGs) respond to cellular stimuli and participate in cellular signaling pathways. The protein products of some IEGs, e.g., c‐jun, are capable of forming dimers and acting as transcriptional regulatory proteins, and have been implicated in apoptosis in both nonneuronal and neuronal cells. In this study, we report a selective and abnormally sustained induction of c‐Jun in cultured hippocampal neurons treated with Aβ. In addition, we describe the lack of induction of c‐Jun in neurons that are relatively resistant to Aβ‐mediated toxicity, and a correspondence between immunoreactivity for c‐Jun and changes in nuclear morphology that are indicative of apoptosis. These data demonstrate that c‐Jun is induced in cultured neurons that undergo Aβ‐mediated apoptosis and suggest that c‐Jun may participate in a cell death program in these neurons.

Journal

Journal of Neurochemistry – Wiley

Published: Jan 1, 1995

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