Abstract
It is currently accepted that epigenetics plays an important role in normal genetics and differentiation, and its failure triggers various diseases such as cancer, aging, metabolic diseases, and abnormal differentiations. The typical mechanism involves the modification of histones and the methylation of DNA. In this study, we investigated the modification of histones in the aged cochlea of mice using immunohistochemistry. Eight mice [C57BL/6(B6)] at the age of 8 weeks (young group) and 132 weeks (aged group) were used. Cochleas were fixed with paraformaldehyde and then decalcified. Hematoxylin-eosin staining was performed for the morphological study using a light microscope. After removing paraffin, the sections were incubated with the primary antibody to acetyl-histone H3 Lys9 or dimethyl-histone H3 Lys9. Confocal scanning microscopy was performed for observation. The degeneration was severest in the spiral ganglion cells and the organ of Corti of the basal turn as determined by light microscopy. Acetylated histone H3 was detected in the spiral ganglion cells and the organ of Corti of the young group, but not in those of the aged group. Dimethylated histone H3 was detected in the spiral ganglion cells and the organ of Corti of the aged group, but not in those of the young group. Acetylation was switched to methylation during ageing. Histone modification is known to have a critical role in neuro-degeneration. Our findings suggest that epigenetic change participates in the process of presbycusis.
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