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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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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

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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

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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.

2022-06-14 | MSV000089650 | MassIVE

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

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 | GSE202664 | GEO

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

2023-05-25 | GSE204841 | GEO

Epigallocatechin Gallate (EGCG) Modulates Senescent Endothelial Cell-Monocyte Communication in Age-Related Vascular Inflammation

Project description:Aging significantly affects intercellular communication between vascular endothelial cells (ECs) and hematopoietic cells, leading to vascular inflammation and age-associated diseases. This study determined how senescent ECs communicate with monocytes, whether extracellular vesicles (EVs) released from senescent ECs affect monocyte functions, and investigated the potential for epigallocatechin-3-gallate (EGCG), a flavonoid in green tea, to reverse these effects. Human umbilical vein endothelial cells (HUVECs) were treated with Etoposide (10 µM, 24h) to induce senescence, followed by EGCG (100 µM, 24h) treatment to evaluate its potential as a senotherapeutic agent. The interaction between ECs and monocytes was analyzed using a co-culture system and direct treatment of monocytes with EC-derived EVs. EGCG reduced senescence-associated phenotypes in ECs, as evidenced by decreased senescence-associated (SA)-β-Gal activity and reversal of Etoposide-induced senescence markers. Monocytes co-cultured with EGCG-treated senescent ECs showed decreased pro-inflammatory responses compared to those co-cultured with untreated senescent ECs. Additionally, senescent ECs produced more EVs than non-senescent ECs. EVs from senescent ECs enhanced lipopolysaccharide (LPS)-induced pro-inflammatory activation of monocytes, whereas EVs from EGCG-treated senescent ECs mitigated this activation, maintaining monocyte activation at normal levels. Our findings reveal that EGCG confers anti-senescent effects via modulation of the senescent EC secretome (including EVs) with the capacity to modify monocyte activation. These findings suggest that EGCG could act as a senotherapeutic agent to reduce vascular inflammation related to aging.

2025-01-18 | GSE286438 | GEO

Epigallocatechin Gallate (EGCG) Modulates Senescent Endothelial Cell-Monocyte Communication in Age-Related Vascular Inflammation

Project description:Epigallocatechin Gallate (EGCG) Modulates Senescent Endothelial Cell-Monocyte Communication in Age-Related Vascular Inflammation

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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

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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

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