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J. Wang, S. Chollangi, A. Saadi, J. Ash; The Gp130/STAT3 Pathway Regulates Adaptive Photostasis. Invest. Ophthalmol. Vis. Sci. 2010;51(13):1680.
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Photostasis is an adaptive response of photoreceptors to the stress of prolonged exposure to bright cyclic light. Animals reared in relatively bright cyclic light have shortened and disorganized outer segments, with decreased rhodopsin packing density in the disk membrane which will reduce efficiency in photon capture by rhodopsin. Our purpose was to identify the molecular mechanisms regulating photostasis in mouse retina.
To test the role of gp130 and STAT3 in photostasis we used mice with retina-specific knockout of either gp130 or STAT3. Two methods, preconditioning mice for 6 days in cyclic bright-light or Intravitreal injections of leukemia inhibitory factor (LIF) were used to induce photostasis. Photostasis was measured by ERG, histology, and expression of phototransduction proteins and mRNA. Chromatin immunoprecipitation was used to analyze STAT3 binding to the promoters of phototransduction related genes.
Both preconditioning with bright light and intravitreal injections of LIF reduced a-waves by ERG, reduced outer segment length, and reduced phototransduction protein and gene expression. In both models STAT3 was strongly activated during photostasis. Deletion of gp130 or STAT3 in the retina blocked the induction of photostasis in both models. Chromatin immunoprecipitation demonstrated STAT3 binding to promoter elements in phototransduction related genes.
Results from this study demonstrated that both gp130 and STAT3 are necessary for adaptive photostasis. STAT3 binding to DNA near phototransduction genes suggests that STAT3 is functioning to suppress their expression resulting in photostasis.
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