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. 2014 Nov 26;9(11):e112996. doi: 10.1371/journal.pone.0112996

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This is an open-access article distributed under the terms of the Creative Commons Public Domain declaration, which stipulates that, once placed in the public domain, this work may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose.

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Stress causes release of glucocorticoid which enhances the expression of CPE-ΔN in embryonic neurons. CPE-ΔN is transported into the nucleus and up-regulates the transcription of FGF2 mRNA and subsequent expression of FGF2 protein. The FGF2 is secreted and binds to FGF2 receptors in neurons to activate AKT and ERK signaling pathways which then mediates the up-regulation of expression of BCL-2, an anti-apoptotic protein. BCL-2 inhibits the caspase cascade leading to a decrease in active caspase-3, the apoptotic executioner, thereby resulting in neuroprotection.