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- W2909937701 abstract "Current literature agrees on the notion that efficient DNA repair favors longevity across evolution. The DNA damage response machinery activates inflammation and type I interferon signaling. Both pathways play an acknowledged role in the pathogenesis of a variety of age-related diseases and are expected to be detrimental for human longevity. Here, we report on the anti-inflammatory molecular make-up of centenarian’s fibroblasts (low levels of IL-6, type 1 interferon beta, and pro-inflammatory microRNAs), which is coupled with low level of DNA damage (measured by comet assay and histone-2AX activation) and preserved telomere length. In the same cells, high levels of the RNAseH2C enzyme subunit and low amounts of RNAseH2 substrates, i.e. cytoplasmic RNA:DNA hybrids are present. Moreover, RNAseH2C locus is hypo-methylated and RNAseH2C knock-down up-regulates IL-6 and type 1 interferon beta in centenarian’s fibroblasts. Interestingly, RNAseH2C locus is hyper-methylated in vitro senescent cells and in tissues from atherosclerotic plaques and breast tumors. Finally, extracellular vesicles from centenarian’s cells up-regulate RNAseH2C expression and dampen the pro-inflammatory phenotype of fibroblasts, myeloid, and cancer cells. These data suggest that centenarians are endowed with restrained DNA damage-induced inflammatory response, that may facilitate their escape from the deleterious effects of age-related chronic inflammation." @default.
- W2909937701 created "2019-01-25" @default.
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- W2909937701 date "2019-01-08" @default.
- W2909937701 modified "2023-10-18" @default.
- W2909937701 title "Genomic stability, anti-inflammatory phenotype, and up-regulation of the RNAseH2 in cells from centenarians" @default.
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- W2909937701 doi "https://doi.org/10.1038/s41418-018-0255-8" @default.
- W2909937701 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6748076" @default.
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- W2909937701 hasPublicationYear "2019" @default.
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