Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/34907
Title: Regulation of caspase activation in axotomized retinal ganglion cells
Authors: Cheung, ZH
Chan, YM
Siu, FK
Yip, HK
Wu, W
Leung, MC 
So, KF
Issue Date: 2004
Publisher: Elsevier
Source: Molecular and cellular neuroscience, 2004, v. 25, no. 3, p. 383-393 How to cite?
Journal: Molecular and cellular neuroscience
Abstract: Transection of the optic nerve initiates massive death of retinal ganglion cells (RGCs). Interestingly, despite the severity of the injury, RGC loss was not observed until several days after axotomy. The mechanisms responsible for this initial lack of RGC death remained unknown. In the current study, immunohistochemical analysis revealed that caspases-3 and -9 activation in the RGCs were not detected until day 3 post-axotomy, coinciding with the onset of axotomy-induced RGC loss. Interestingly, elevated Akt phosphorylation was observed in axotomized retinas during the absence of caspase activation. Inhibiting the increase in Akt phosphorylation by intravitreal injection of wortmannin and LY294002, inhibitors of PI3K, resulted in premature nuclear fragmentation, caspasess-3 and -9 activation in the RGCs were not detected until day 3 post-axotomy, coinciding with the onset of axotomy-induced RGC loss. Interestingly, elevated Akt phosphorylation was observed in axotomized retinas during the absence of caspase activation. Inhibiting the increase in Akt phosphorylation by intravitreal injection of wortmannin and LY294002, inhibitors of PI3K, resulted in premature nuclear fragmentation, caspasess-3 and -9 activation in the ganglion cell layer. Our findings thus indicate that the PI3K/Akt pathway may serve as an endogenous regulator of caspase activation in axotomized RGCs, thereby, contributing to the late onset of RGC death following axotomy.
URI: http://hdl.handle.net/10397/34907
ISSN: 1044-7431
DOI: 10.1016/j.mcn.2003.11.001
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