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Repetitive element transcript accumulation is related to inflammaging in humans

ABSTRACT: Repetitive element transcript accumulation is related to inflammaging in humans

PROVIDER: PRJNA1095453 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28532100_1.fastq.gz	Fastqsanger.gz
	SRR28532100_2.fastq.gz	Fastqsanger.gz
	SRR28532101_1.fastq.gz	Fastqsanger.gz
	SRR28532101_2.fastq.gz	Fastqsanger.gz
	SRR28532102_1.fastq.gz	Fastqsanger.gz

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Repetitive element transcript accumulation is related to inflammaging in humans

Project description:Inflammation is an established feature of many age-related diseases, and growing evidence implicates transcripts from repetitive elements in inflammatory signaling with aging. We generated transcriptomic (RNA-seq) and whole-genome bisulfite sequencing (WGBS, for methylation) data on frozen/biobanked peripheral blood mononuclear cells from middle-aged and older adults, as well as younger and older adults before and after an exercise intervention, to evaluate correlations among repetitive elements and inflammation, along with methylation of repetitive elements.

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Repetitive element transcript accumulation is associated with inflammaging in humans.

Project description:Chronic, low-grade inflammation increases with aging, contributing to functional declines and diseases that reduce healthspan. Growing evidence suggests that transcripts from repetitive elements (RE) in the genome contribute to this "inflammaging" by stimulating innate immune activation, but evidence of RE-associated inflammation with aging in humans is limited. Here, we present transcriptomic and clinical data showing that RE transcript levels are positively related to gene expression of innate immune sensors, and to serum interleukin 6 (a marker of systemic inflammation), in a large group of middle-aged and older adults. We also: (1) use transcriptomics and whole-genome bisulfite (methylation) sequencing to show that many RE may be hypomethylated with aging, and that aerobic exercise, a healthspan-extending intervention, reduces RE transcript levels and increases RE methylation in older adults; and (2) extend our findings in a secondary dataset demonstrating age-related changes in RE chromatin accessibility. Collectively, our data support the idea that age-related RE transcript accumulation may play a role in inflammaging in humans, and that RE dysregulation with aging may be due in part to upstream epigenetic changes.

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