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Courtney Bricker-Anthony, Tonia S Rex; Cell Death after Ocular Blast Trauma is Primarily Non-Apoptotic. Invest. Ophthalmol. Vis. Sci. 2014;55(13):367.
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To determine what cell death pathways are activated after ocular blast trauma.
We exposed the left eyes of 3 month-old mice to a single, 26psi overpressure airwave. Mice were collected at 1, 3, 7, 14, and 28 days post-injury. All eyes were cryo-embedded, sectioned and labeled with antibodies against caspase 1, RIP, RIP3, cleaved caspase-3, calpain, cathepsin D, and TUNEL.
The peak of cell death was identified by TUNEL and this time point was then used as a reference for all cell death marker analyses. No changes in calpain or cathepsin D were detected post-blast. Rare photoreceptors were labeled with the apoptosis marker, cleaved caspase 3 and some condensed nuclei were detected in resin tissue sections. Labeling with the pyroptosis marker, caspase 1, was present in the inner retina post-blast. RIP, a marker for necroptosis, was localized to the Müller glia and inner plexiform layer in normal and post-blast retina. RIP3 was detected in the inner plexiform layer and in a small number of cells in the retinal ganglion cell layer and inner nuclear layer in controls. After blast, RIP3 was also present in the outer nuclear layer.
These results suggest that blast injury causes cell death via multiple pathways. The majority of photoreceptor cell death appears to be through necroptosis, although some apoptosis also occurs. The inner retina cells may die via necroptosis and pyroptosis.
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