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Tingting Jiang, Qing Chang, Gezhi Xu; Epigenetic changes in melatonin-Mediated Cytoprotection against Hyperglycemic Injury in Müller Cells. Invest. Ophthalmol. Vis. Sci. 2014;55(13):1054.
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© ARVO (1962-2015); The Authors (2016-present)
Inflammation plays important roles in the development of diabetic retinopathy (DR). The aim of this study was to investigate the epigenetic modulation by melatonin to attenuate inflammatory response in Müller cells under hyperglycemic condition.
Primary cultured Müller cells were divided into several groups, treated with either high glucose medium (containing 30 mM glucose) alone or combined with melatonin (0.1 mM) for various time. Melatonin was dissolved in dimethylsulfoxide (DMSO) and the stock solutions were added directly to the serum-free culture media. In the osmotic control group, cells were treated with medium containing 5.5 mM glucose and 24.5 mM mannitol. TNFα, IL1βexpressions were measured by Real-time PCR. HDAC4, HDAC5, AcH3K9 and AcH4K5mRNA and protein expressions were measured by Real-time PCR and Western Blot. Data were analyzed with the SPSS 16 software (IBM). Means ± SD were calculated for each group. For multiple comparisons, one-way ANOVA followed by Tukey's multiple comparison tests were used. Differences were considered statistically significant when p-value was less than 0.05.
TNFαand IL1βexpressions were upregulated by high glucose stimulation compared with the control group (P<0.05) and melatonin attenuated the expressions (P<0.05). Under hyperglycemic condition, the levels of HDAC4 and HDAC5 were reduced, while AcH3K9 and AcH4K5 levels were elevated (P<0.05). However, melatonin reversed the effects. (P<0.05)
These findings suggest epigenetic regulation by melatonin may contribute to its anti-inflammatory effect on DR.
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