Purchase this article with an account.
Y.–D. Bifrare, S.L. Leib, T.J. Wolfensberger; Lamin a Cleavage in Photoreceptors Due to Experimental Retinal Detachment in an Adult and Infant Rat Model . Invest. Ophthalmol. Vis. Sci. 2006;47(13):4574.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Retinal detachment leads to photoreceptor degeneration and chronic visual loss if left untreated. The molecular mechanisms are still incompletely understood but include apoptotic processes. Lamin cleavage contributes to chromatin condensation and nuclear shrinkage, two processes involved in the execution of apoptosis. Lamin A is exclusively cleaved by caspase–6. There is an ongoing controversy on the role of caspase–3 in the activation of caspase–6.
Here we investigated the functional involvement of caspase–6 and caspase–3 in photoreceptor cell death during retinal detachment.
Adult and 20 day old infant rats were anesthetized and retinas were detached by subretinal injection of saline in the left eye while the right eye was used as a control. Immunohistochemistry for activated caspase–3 and cleaved lamin A was performed using a polyclonal anti–rabbit antibody. Cells staining positively were counted per visual field (x40) and a mean per eye was calculated.
Cleaved lamina A, but not activated caspase–3 was documented in all detached retinas, while no signal was detected in adherent control retinas.
We established a model of retinal detachment in infant rats with the occurrence of photoreceptor cell death as previously documented in the adult model. In this model we demonstrated that caspase–6, through cleavage of its substrate lamin A, contributes to cell death in the outer granular layer in the absence of caspase–3 activation.
This PDF is available to Subscribers Only