Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 115, Issue 29, Pages 7611-7616Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1800656115
Keywords
inflammation; aging; brain; H3K27ac; gene-body acetylation
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Funding
- China Ministry of Science and Technology [2015CB964803, 2016YFE0108700, 2016YFA0101800]
- National Natural Science Foundation of China [91749205, 31210103916, 91519330]
- Chinese Academy of Sciences [XDB19020301, XDA01010303]
- National Institutes of Health [P30AG10161, R01AG15819, R01AG17917]
- Science and Technology Commission of Shanghai Municipality Grant [16XD1400500]
- NATIONAL INSTITUTE ON AGING [RF1AG015819, R01AG017917, P30AG010161, R01AG015819] Funding Source: NIH RePORTER
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Brain inflammaging, a low-grade and chronic inflammation, is a major hallmark for aging-related neurodegenerative diseases. Here, by profiling H3K27ac and gene expression patterns in human and mouse brains, we found that age-related up-regulated (Age-Up) and down-regulated (Age-Down) genes have distinct H3K27ac patterns. Although both groups show promoter H3K27ac, the Age-Up genes, enriched for inflammation-related functions, are additionally marked by broad H3K27ac distribution over their gene bodies, which is progressively reduced during aging. Age-related gene expression changes can be predicted by gene-body H3K27ac level. Contrary to the presumed transcription activation function of promoter H3K27ac, we found that broad gene-body hyper H3K27ac suppresses overexpression of inflammaging genes. Altogether, our findings revealed opposite regulations by H3K27ac of Age-Up and Age-Down genes and a mode of broad gene-body H3K27ac in repressing transcription.
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