Caspase-2 Mediates Site-Specific Retinal Ganglion Cell Death After Blunt Ocular Injury | Zendy

Chloe N. Thomas | Zendy; Adam Thompson | Zendy; Eleanor McCance | Zendy; Martin Berry | Zendy; Ann Logan | Zendy; Richard J. Blanch | Zendy; Zubair Ahmed | Zendy

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Caspase-2 Mediates Site-Specific Retinal Ganglion Cell Death After Blunt Ocular Injury

Author(s) -

Chloe N. Thomas,

Adam Thompson,

Eleanor McCance,

Martin Berry,

Ann Logan,

Richard J. Blanch,

Zubair Ahmed

Publication year - 2018

Publication title -

investigative ophthalmology and visual science

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.935

H-Index - 218

eISSN - 1552-5783

pISSN - 0146-0404

DOI - 10.1167/iovs.18-24045

Subject(s) - retinal ganglion cell , retina , ophthalmology , outer nuclear layer , electroretinography , retinal degeneration , photoreceptor cell , programmed cell death , retinal , caspase 3 , biology , blunt trauma , medicine , pathology , apoptosis , surgery , neuroscience , biochemistry

Ocular trauma is common in civilian and military populations. Among other injuries, closed globe blunt ocular trauma causes acute disruption of photoreceptor outer segments (commotio retinae) and retinal ganglion cell (RGC) death (traumatic optic neuropathy [TON]), both of which permanently impair vision. Caspase-2-dependent cell death is important and evidenced in models of RGC degeneration. We assessed the role of caspase-2 as a mediator of RGC and photoreceptor death in a rat blunt ocular trauma model.

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