%0 Journal Article
%T Lens Injury Has a Protective Effect on Photoreceptors in the RCS Rat
%A Peter Heiduschka
%A Daniel Renninger
%A Dietmar Fischer
%A Adrienne M¨¹ller
%A Sabine Hofmeister
%A Ulrich Schraermeyer
%J ISRN Ophthalmology
%D 2013
%R 10.1155/2013/814814
%X Lens injury induced activation of retinal glia, and subsequent release of ciliary neurotrophic factor (CNTF) and leukaemia inhibitory factor (LIF) potently protect axotomised retinal ganglion cells from apoptosis and promotes axon regeneration in the injured optic nerve. The goal of the current study was to investigate if similar effects may also be applicable to rescue photoreceptors from degeneration in a model of retinitis pigmentosa. Lens injury was performed in the Royal College of Surgeons (RCS) rats at the age of one month. The survival of photoreceptors was evaluated histologically, and retinal function was analysed by electroretinography (ERG). Expression of CNTF was also analysed. Lens injury significantly enhanced the survival of photoreceptors 1 month after surgery compared to untreated controls, which was associated with an enhanced ERG response. In addition, lens injury significantly protected photoreceptors from degeneration in the contralateral eye, although to a much lesser extent. We could show that lens injury is sufficient to transiently delay the degeneration of photoreceptors in the RCS rat. The observed neuroprotective effects may be at least partially mediated by an upregulation of CNTF expression seen after lens injury. 1. Introduction It has recently been shown that lens injury or intravitreal applications of lens-derived ¦Â/¦Ã-crystallins potently protect axotomised retinal ganglion cells (RGCs) from cell death and stimulate axon regeneration in the injured optic nerve [1¨C5]. All treatments induce an activation of retinal astrocytes and M¨¹ller cells, which subsequently upregulate and release the cytokines ciliary neurotrophic factor (CNTF) and leukaemia inhibitory factor (LIF) [6¨C10]. The strong neuroprotective effects of lens injury are completely absent in CNTF/LIF double knockout mice, demonstrating that both cytokines act as essential key mediators [9, 11]. Similar to these factors, interleukin 6 also promotes neuroprotection [12]. The purpose of the current study was to investigate whether lens injury is also sufficient to protect photoreceptors from degeneration. As a model, we chose the Royal College of Surgeons (RCS) rat, which is a commonly used model of retinal degeneration, in particular retinitis pigmentosa. The cells of the retinal pigment epithelium (RPE) are not capable of phagocytosing photoreceptor outer segments due to a mutation in the Mertk gene. This leads to a gradual degeneration of the photoreceptors starting at the time point of eye opening (i.e., approximately at P20) and being completed at the age of 3
%U http://www.hindawi.com/journals/isrn.ophthalmology/2013/814814/