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R. V. Rajala, Y. Z. Le, Y. L. Lee, A. Rajala, R. C. Kahn, M. Tanito; Deletion of the Insulin Receptor in Rod Photoreceptor Cells Results in Light-Induced Retinal Degeneration. Invest. Ophthalmol. Vis. Sci. 2007;48(13):4653.
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We previously demonstrated the light-induced tyrosine phosphorylation of retinal insulin receptor (IR) and localized the light effect to the photoreceptor neurons. We also observed that light stress induced the tyrosine phosphorylation of the IR in rod outer segments (ROS). To investigate the significance of the IR in rod photoreceptors, we disrupted the IR gene specifically in mouse rod photoreceptors and characterized the effect on retinal function and morphology.
Rod-specific IR knockout mice were generated by mating mouse opsin promoter controlled Cre-expressing mice with floxed IR mice. Deletion of the IR in ROS isolated from rod photoreceptors was demonstrated by Western blot analysis. These mice were exposed to constant bright light stress and photoreceptor structural and functional integrity was measured by quantitative morphometry [outer nuclear layer (ONL) thickness] and electroretinography (ERG).
Specifically disruption of IR expression in rod photoreceptors significantly decreased ERG amplitudes and ONL thickness in mice exposed to bright light stress.
Loss of the IR rod photoreceptor cells increases their susceptibility to light-induced apoptosis and suggests that the IR pathway is important for photoreceptor survival and maintenance. Activation of the IR may be an essential element of photoreceptor neuroprotection.
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