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Updated: May 9, 2026
09:29
Isolation of Intermediate Filament Proteins from Multiple Mouse Tissues to Study Aging-associated Post-translational Modifications
Published on: May 18, 2017
Tissue-specific modification of clock methylation in aging mice.
1Department of Pharmacology, Xuanwu Hospital of Capital Medical University, Beijing, People's Republic of China.
European Review for Medical and Pharmacological Sciences
|July 24, 2013
Summary
Aging alters DNA methylation in clock genes, impacting circadian rhythms. This study reveals tissue-specific changes in methylation patterns in older mice, contributing to age-related circadian dysfunction.
Area of Science:
- Chronobiology
- Molecular Biology
- Gerontology
Background:
- Circadian rhythms exhibit age-related changes.
- The molecular mechanisms driving these alterations are not fully understood.
Purpose of the Study:
- To investigate age-related DNA methylation changes in clock genes.
- To determine if these epigenetic modifications contribute to circadian dysfunction in aging animals.
Main Methods:
- Examined DNA methylation of clock gene promoters.
- Utilized methylation-specific polymerase chain reaction (MSP) assay.
- Analyzed tissues including stomach, kidney, striatum, and spleen.
Main Results:
- Tissue-specific patterns of clock gene methylation were observed.
- Decreased methylation frequency at the Per1 promoter in the stomach of older mice.
- Increased methylation frequency at Cry1, Bmal2, and Npas2 promoters in the spleen of older mice.
Conclusions:
- DNA methylation plays a role in age-related circadian rhythm alterations.
- Specific clock genes and tissues are affected by age-related epigenetic changes.
- Findings suggest DNA methylation contributes to dysfunction in certain slave oscillators during aging.
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