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

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

PROVIDER: PRJNA836900 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19159300.fastq.gz	Fastqsanger.gz
	SRR19159286.fastq.gz	Fastqsanger.gz
	SRR19159287.fastq.gz	Fastqsanger.gz
	SRR19159288.fastq.gz	Fastqsanger.gz
	SRR19159289.fastq.gz	Fastqsanger.gz

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Similar Datasets

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

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

| PRJNA844084 | ENA

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

Project description:TXNRD1 drives innate immune response in senescent cells and promotes age-associated inflammation II

| PRJNA842434 | ENA

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.

2022-06-14 | MSV000089650 | MassIVE

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

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

2023-05-25 | GSE204841 | GEO

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

2023-05-25 | GSE202664 | GEO

Whole-Body Senescent Cell Clearance Alleviates Age-Related Brain Inflammation and Cognitive Impairment in Mice

Project description:Cellular senescence is characterized by an irreversible cell cycle arrest and a pro-inflammatory senescence-associated secretory phenotype (SASP), which is a major contributor to aging and age-related diseases. Clearance of senescent cells has been shown to improve brain function in mouse models of neurodegenerative diseases. However, it is still unknown whether senescent cell clearance alleviates cognitive dysfunction during the aging process. To investigate this, we first conducted single-nuclei and single-cell RNA-seq in the hippocampus from young and aged mice. We observed an age-dependent increase in p16Ink4a senescent cells, which was more pronounced in microglia and oligodendrocyte progenitor cells and characterized by a SASP. We then aged INK-ATTAC mice, in which p16Ink4a-positive senescent cells can be genetically eliminated upon treatment with the drug AP20187 and treated them either with AP20187 or with the senolytic cocktail Dasatinib and Quercetin. We observed that both strategies resulted in a decrease in p16Ink4a exclusively in the microglial population, resulting in reduced microglial activation and reduced expression of SASP factors. Importantly, both approaches significantly improved cognitive function in aged mice. Our data provide proof-of-concept for senolytic interventions’ being a potential therapeutic avenue for alleviating age-associated cognitive impairment.

2021-02-06 | GSE161340 | GEO

Regulatory innate lymphoid cells control innate intestinal inflammation

Project description:Regulatory innate lymphoid cells control innate intestinal inflammation

| PRJNA394222 | ENA

Whole-Body Senescent Cell Clearance Alleviates Age-Related Brain Inflammation and Cognitive Impairment in Mice

Project description:Whole-Body Senescent Cell Clearance Alleviates Age-Related Brain Inflammation and Cognitive Impairment in Mice

| PRJNA677926 | ENA

Project description:To understand the age-related retinal gene changes, gene transcription profiles of neural retinal tissues from young adult (3-month) mice and old (20-month) mice were investigated by microarray. With age, 632 genes were up-regulated and 429 genes were down-regulated in the retina. Functional annotation showed that genes linked to immune responses and to tissue stress/injury responses were most modified by old age. Significant numbers of gene involved in the innate immune response including leukocyte activation, chemotaxis, endocytosis, complement activation, phagocytosis and myeloid cell differentiation were up-regulated and only a few were down-regulated. Increased microglial and complement activation in the aging retina was further confirmed by confocal microscopy of retinal tissues. The results suggest that retinal aging is accompanied with activation of a number of local inflammatory responses. A modified form of low-grade chronic inflammation (para-inflammation) characterizes these aging changes and involves mainly the innate immune system. Para-inflammation per se may be beneficial to normal retinal physiology in aging by promoting retinal homeostasis; conversely, dysreulation of the para-inflammation response may contribute to the pathogenesis of age-related retinal degeneration. Six young (3-month) and six old (20-month) mice were used for microarray study. Total RNA from each sample were extracted and undergone quality control analysis. RNA from 3 mice of the same group were then pooled together for gene array experiment.

2009-12-31 | E-GEOD-17423 | biostudies-arrayexpress

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.

| S-EPMC6519963 | biostudies-literature

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