Caspase-3 activation, rather than increased mRNA expression, mediates secondary retinal ganglion cell death following optic nerve transection in vivo.
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May implicate post-transcriptional caspase-3 regulation in experimental retinal injury; hypothesis-generating for optic neuropathy therapies.
Recently, we have shown that inhibition of caspase-3-like caspases is the most effective treatment strategy to protect adult rat retinal ganglion cells from secondary death following optic nerve transection. In the present study, we localized active caspase-3 in axotomized retinal ganglion cells in vivo and demonstrated a co-localization of the active p20 fragment and TUNEL-staining in some of these cells. In line with this, we detected an enhanced cleavage and activity of caspase-3 protein in retinal tissue after lesion, while caspase-3 mRNA expression remained unchanged. These data suggest caspase-3 as an important mediator of secondary retinal ganglion cell death following axotomy in vivo.
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Kermer et al. (1999) studied this question.
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