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R. Zhang, P. Chen, H. Arnouk, X. Yang, E. Oh, P. Wood, W. Hrushesky, R. Davis, W. Jahng; Melatonin Protects Retina From Constant Light Induced Damage via Microtubule Stabilization. Invest. Ophthalmol. Vis. Sci. 2008;49(13):788.
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Mechanisms that are involved in constant light induced retina degeneration remain to be largely unknown. Melatonin, synthesized in pineal gland and also in retina during the dark phase of photoperiod, has several functions and mostly regarded as a free radical scavenger. In this study, we investigated proteins that are involved in the process of light induced retina degeneration and examined whether dramatically decreased level of melatonin in light phase is the major reason causing damage in retina in constant light exposed eyes. We further explored the molecular mechanism through which melatonin protects retina from the light.
Three groups of mice were used in our experiment. First group were maintained on a 12hr light/dark cycle; second group were kept in room light constantly for 10 days, while the third group were treated with melatonin and maintained in constant room light for 10 days. We then performed 2D gel electrophoresis to find retinal proteins that expressions were changed upon constant room light. MALDI-TOF-TOF mass spectrometry analysis was used to identify proteins. In order to further explore mechanisms through which melatonin protects retina from light induced damage, we compared protein profiles between melatonin treated and untreated groups that are exposed to constant light to identify proteins that are regulated by melatonin.
The levels of several proteins in the retina were increased during constant light exposure. Mass spectrometry analysis identified proteins including heterogeneous nuclear ribonucleoprotein H, beta-crystallin, alpha-crystallin, glutamine synthase, and ATP synthase. Proteins that are found to be down regulated are vimentin and tubulin-beta. Interestingly, in constant light-exposed mice with melatonin treatment, vimentin and tubulin-beta are up-regulated to their original levels.
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