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Author Correction: L1 drives IFN in senescent cells and promotes age-associated inflammation.

ABSTRACT: An Amendment to this paper has been published and can be accessed via a link at the top of the paper.

SUBMITTER: De Cecco M

PROVIDER: S-EPMC7017651 | biostudies-literature | 2019 Aug

REPOSITORIES: biostudies-literature

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Author Correction: L1 drives IFN in senescent cells and promotes age-associated inflammation.

De Cecco Marco M Ito Takahiro T Petrashen Anna P AP Elias Amy E AE Skvir Nicholas J NJ Criscione Steven W SW Caligiana Alberto A Brocculi Greta G Adney Emily M EM Boeke Jef D JD Le Oanh O Beauséjour Christian C Ambati Jayakrishna J Ambati Kameshwari K Simon Matthew M Seluanov Andrei A Gorbunova Vera V Slagboom P Eline PE Helfand Stephen L SL Neretti Nicola N Sedivy John M JM

Nature 20190801 7767

An Amendment to this paper has been published and can be accessed via a link at the top of the paper. ...[more]

PMID: 31296937

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L1 drives IFN in senescent cells and promotes age-associated inflammation.

Project description:Retrotransposable elements are deleterious at many levels, and the failure of host surveillance systems for these elements can thus have negative consequences. However, the contribution of retrotransposon activity to ageing and age-associated diseases is not known. Here we show that during cellular senescence, L1 (also known as LINE-1) retrotransposable elements become transcriptionally derepressed and activate a type-I interferon (IFN-I) response. The IFN-I response is a phenotype of late senescence and contributes to the maintenance of the senescence-associated secretory phenotype. The IFN-I response is triggered by cytoplasmic L1 cDNA, and is antagonized by inhibitors of the L1 reverse transcriptase. Treatment of aged mice with the nucleoside reverse transcriptase inhibitor lamivudine downregulated IFN-I activation and age-associated inflammation (inflammaging) in several tissues. We propose that the activation of retrotransposons is an important component of sterile inflammation that is a hallmark of ageing, and that L1 reverse transcriptase is a relevant target for the treatment of age-associated disorders.

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TXNRD1 drives innate immune response in senescent cells and promotes age-associated inflammation

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TXNRD1 drives innate immune response in senescent cells and promotes age-associated inflammation

Project description:Sterile inflammation, also known as inflammaging, is a hallmark of tissue ageing. Cellular senescence contributes to tissue aging in part through secretion of proinflammatory factors known as senescence-associated secretory phenotype (SASP). Thioredoxin reductase 1 (TXNRD1) genetic variability is associated with aging and age-associated phenotypes such as late-life survival, activity of daily living, and physical performance at old age. TXNRD1 role in regulating tissue ageing has been attributed to its enzymatic role in regulating cellular redox. Here we show that TXNRD1 drives SASP and inflammaging through the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) innate immune response pathway independently of its enzymatic activity. TXNRD1 localizes to cytoplasmic chromatin fragment and interacts with cGAS in a senescence status dependent manner. TXNRD1 enhances the enzymatic activity of cGAS. TXNRD1 and its interaction with cGAS is necessary for the SASP. TXNRD1 is required for both the tumor-promoting and immune-surveillance functions of senescent cells, which are mediated by SASP in vivo in mouse models. Treatment of aged mice with an TXNRD1 inhibitor that disrupts its interaction with cGAS, but not an inhibitor of its enzymatic activity, downregulated inflammaging in several tissues. In summary, our results report TXNRD1 promotes inflammaging via the innate immune response. They indicate that TXNRD1 and cGAS interaction is a relevant target for selectively suppressing inflammaging.

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Project description:Sterile inflammation, also known as “inflammaging”, is a hallmark of tissue ageing. Cellular senescence contributes to tissue aging in part through secretion of proinflammatory factors known as senescence-associated secretory phenotype (SASP). Thioredoxin reductase 1 (TXNRD1) genetic variability is associated with aging and age-associated phenotypes such as late-life survival, activity of daily living, and physical performance at old age. TXNRD1’s role in regulating tissue ageing has been attributed to its enzymatic role in reducing reactive oxygen species. Here we show that TXNRD1 drives SASP and inflammaging through the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) innate immune response pathway independent of its enzymatic activity

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Author Correction: Diversity in gut bacterial community of school-age children in Asia.

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