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Abdoulaye Sene, Jonathan B Lin, Doug Cox, Nicole Zapata, Andrea Santeford, William A Frazier, Rajendra S Apte; Selective Targeting of Rod Photoreceptors in Inflammation-Induced Neurodegeneration. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):5431.
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© ARVO (1962-2015); The Authors (2016-present)
Dysfunction or death of photoreceptors is a common feature of many retinal disorders including AMD, exudative and rhegmatogenous retinal detachment, diabetic retinopathy, retinopathy of prematurity, and retinitis pigmentosa. We investigated regulatory mechanisms responsible for photoreceptor survival in the context of inflammation-induced degeneration.
We used an experimental model of retinal detachment to elucidate the regulatory pathways involved in photoreceptor cell death. Surgical separation of the neurosensory retina from the underlying RPE was performed on the following: C57BL6 (wt), pro- or anti-inflammatory cytokine-deficient, and several cell-surface marker-depleted mice. We analyzed the time course of apoptotic cell death in the retina by TUNEL staining. We also used Electroretinogram (ERG) analysis to evaluate rod and cone responses after neurosensory detachment.
We found that infiltrating macrophages induced selective photoreceptor apoptotic death while other retinal cells were effectively protected. In addition, co-immunostaining of photoreceptor cells with specific markers revealed that rod cells were more susceptible to cell death than cone cells. Electroretinogram (ERG) analysis confirmed that only rod (scotopic) responses were affected while cone (photopic) responses remained intact. In addition, we demonstrated that neurosensory detachment in NRL-/- mice (pure cone retina) had no effect on photoreceptor survival.
We have demonstrated that rod and cone photoreceptors exhibit differential vulnerability to inflammation-induced cell death. These data suggested that in response to retinal injury, photoreceptor cells might activate divergent intrinsic programs that determine their fate.
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