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Large-scale Chemical Screen Identifies a Geroprotective Role of Gallic Acid in Premature Aging [ATAC-seq]

ABSTRACT: Gallic acid (GA) is a natural phenolic compound with antioxidant, anti-inflammatory, and antineoplastic properties. Previous studies also revealed that GA supplementation inhibit the decline of rat embryonic and rejuvenate the immune function in D-gal-induced aging accelerated mice. However, the role of GA in regulating senescence of human premature aging stem cells is unknown. We have demonstrated that GA showed beneficial effects in alleviating human mesenchymal stem cell (hMSC) senescence: (1) GA alleviated senescence by promoting stem cell self-renewal ability and down-regulating the expression of aging markers, including P16 and P21, in Werner syndrome (WS) hMSCs; (2) High levels of reactive oxygen species in total cell as well as mitochondria were both rescued by GA treatment; (3) GA also maintained epigenetic features, enhanced cell stemness, and improved mitochondrial homeostasis in WS hMSCs. Our data provide substantial evidence supporting that GA is a promising candidate agent to

ORGANISM(S): Homo sapiens

PROVIDER: GSE181444 | GEO | 2021/08/05

REPOSITORIES: GEO

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Large-scale Chemical Screen Identifies a Geroprotective Role of Gallic Acid in Premature Aging [RNA-seq]

Project description:Gallic acid (GA) is a natural phenolic compound with antioxidant, anti-inflammatory, and antineoplastic properties. Previous studies also revealed that GA supplementation inhibit the decline of rat embryonic and rejuvenate the immune function in D-gal-induced aging accelerated mice. However, the role of GA in regulating senescence of human premature aging stem cells is unknown. We have demonstrated that GA showed beneficial effects in alleviating human mesenchyme stem cell(hMSC) senescence: (1) GA alleviated senescence by promoting stem cell self-renewal ability and down-regulating the expression of aging markers, including P16 and P21, in Werner syndrome(WS) hMSCs; (2) High levels of reactive oxygen species in total cell as well as mitochondria were both rescued by GA treatment; (3) GA also maintained epigenetic features, enhanced cell stemness, and improved mitochondrial homeostasis in WS hMSCs. Our data provide substantial evidence supporting that GA is a promising candidate agent to

2021-06-25 | GSE175733 | GEO

Chemical Screen Identifies a Geroprotective Role of Quercetin in Premature and Physiological Aging

Project description:Aging increases the vulnerability to various diseases. The main goal of aging research is to find therapies that attenuate aging and alleviate aging-related diseases. In this study, we screened a nature product library for geroprotective compounds using Werner syndrome (WS) human mesenchymal stem cells (hMSCs), a premature aging model that we recently established. Ten candidate targets were identified and quercetin was further investigated due to its leading effects. Mechanistic studies revealed that in WS hMSCs, quercetin alleviated senescence via the enhancement of cell proliferation and the restoration and differentiation of heterochromatin architecture. RNA-seq analysis uncovered that quercetin and Vitamin C exerted geroprotective effects through different mechanisms. Besides WS hMSCs, quercetin also attenuated cellular senescence in Hutchinson-Gilford progeria syndrome (HGPS), physiological-aging and replicative-senescent hMSCs. More importantly, quercetin significantly improved the exercise endurance of old C57Bl/6 mice. Taken together, our study identifies quercetin as a geroprotective agent against premature and physiological aging, providing a novel therapeutic intervention for treating premature aging and promoting healthy aging.

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Expression profiling of skin fibroblast and iPSC from Werner Syndrome

Project description:The premature aging disorder Werner Syndrome (WS) is characterized by early onset of aging phenotypes resembling natural aging. In most WS patients there are mutations in the DNA helicase WRN, an enzyme important in maintaining genome stability and telomere replication. Interestingly, its clinical manifestations reflect a severe degree of deterioration for connective tissue, whereas the central nervous system is less affected. We suggest that the varied vulnerability to aging is regulated by an unknown mechanism that protects specific lineages of stem cells from premature senescence. To address this problem, we reprogrammed patient skin fibroblasts to induced pluripotent stem cells (iPSC). The expression profile for the differentiated normal and WS fibroblasts and undifferentiated iPSC were compared. A distinct expression profile was found between normal and WS fibroblasts, however, few changes of gene expression were found in iPSC. Our findings suggest an erasure of aging phenotype associated with WS in reprogrammed iPSC. Human normal and WS skin fibroblasts were reprogrammed to induced pluripotent stem cells (iPSC). These samples, before and after reprogramming, were analyzed for the change of gene expression profile.

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NAD+ augmentation restores mitophagy and limits accelerated aging in Werner syndrome

Project description:Metabolic dysfunction is a primary feature of Werner syndrome (WS), a human premature aging disease caused by mutations in the gene encoding the Werner (WRN) DNA helicase. WS patients exhibit severe metabolic phenotypes, but the underlying mechanisms are not understood, and whether the metabolic deficit can be targeted for therapeutic intervention has not been determined. Here we report impaired mitophagy and depletion of NAD+, a fundamental ubiquitous molecule, in WS patient samples and WS invertebrate models. WRN regulates transcription of a key NAD+ biosynthetic enzyme nicotinamide nucleotide adenylyltransferase 1 (NMNAT1). NAD+ repletion restores NAD+ metabolic profiles and improves mitochondrial quality through DCT-1 and ULK-1-dependent mitophagy. At the organismal level, NAD+ repletion remarkably extends lifespan and delays accelerated aging, including stem cell dysfunction, in C. elegans and Drosophila melanogaster models of WS. Our findings suggest that accelerated aging in WRN syndrome is mediated by impaired mitochondrial function and mitophagy, and that bolstering cellular NAD+ levels counteracts WS phenotypes.

2020-01-13 | PXD015644 | Pride

Expression profiling of skin fibroblast and iPSC from Werner Syndrome

2013-07-11 | GSE48761 | GEO

Expression data from Werner syndrome iPSCs

Project description:Werner syndrome (WS) is a premature aging disorder characterized by chromosomal instability and cancer predisposition. Mutations in WRN are responsible for the disease and cause telomere dysfunction, resulting in accelerated aging. In the present study, we describe the effects of long-term culture on WS iPSCs, which acquired and maintained infinite proliferative potential for self-renewal over 2 years. After long-term cultures, WS iPSCs exhibited stable undifferentiated states and differentiation capacity, and premature upregulation of senescence-associated genes in WS cells was completely suppressed in WS iPSCs despite WRN deficiency. We used microarrays to examine whether global gene expression profile of WS iPSCs is similar to that of normal iPSCs and human ESCs, as well as premature senescence phenotype is suppressed by reprogramming.

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Transcriptional profile Lactobacillus plantarum WCFS1 : 1.5mM gallic acid (GA) treated cells

Project description:Whole genome transcriptional profiling was used to characterize the response of Lactobacillus plantarum WCFS1 human isolate during challenge with 1.5 mM gallic acid (GA). Twelve independent experiments were performed and mixed at random in groups of four for total of three RNA samples. The transcriptional profile reveals a massive induction of genes involved in transport and decarboxilation of gallic acid.

2015-10-15 | GSE63728 | GEO

Transcriptional profile Lactobacillus plantarum WCFS1: 15 mM gallic acid (GA) treated cells

Project description:Whole genome transcriptional profiling was used to characterize the response of Lactobacillus plantarum WCFS1 human isolate during challenge with gallic acid (GA). Twelve independent experiments were performed and mixed at random in groups of four for total of three RNA samples. The transcriptional profile reveals a massive induction of genes involved in transport and decarboxilation of gallic acid.

2015-10-15 | GSE56997 | GEO

4E-BP1 counteracts human stem cell senescence via maintaining mitochondrial homeostasis

Project description:Although the mTOR-4E-BP1 signaling pathway is implicated in aging and aging-related disorders, the role of 4E-BP1 in regulating human stem cell homeostasis remains largely unknown. Here, we report that the expression of 4E-BP1 decreases along with the senescence of human mesenchymal stem cells (hMSCs). Genetic inactivation of 4E-BP1 in hMSCs accelerates cellular senescence, compromises mitochondrial respiration and increases mitochondrial ROS production. Mechanistically, the absence of 4E-BP1 destabilizes proteins in mitochondrial respiration complexes, especially several key subunits of the complex III including UQCRC2. Ectopic expression of 4E-BP1 attenuates mitochondrial abnormalities and alleviates cellular senescence in 4E-BP1-deficient hMSCs as well as in physiologically aged hMSCs. These findings together demonstrate that 4E-BP1 functions as a geroprotector to alleviate human stem cell senescence and maintain mitochondrial homeostasis, particularly for the mitochondrial respiration complex III and provide a new potential target to counteract human stem cell senescence.

2023-05-10 | PXD033301 | Pride

Expression data from 5azaC- or gallic acid-treated human lung cancer H1299 cell line

Project description:Gallic acid (also known as 3,4,5-trihydroxybenzoic acid, GA), a naturally occurring phenolic acid, is a major constituent of tea and red wine. It has been demonstrated that GA possess anti-cancer activities. We found the epigenetic effect of GA in tobacco-associated human cancer cell lines. In this dataset, we include the expression array data from human lung cancer H1299 cell line with or without the treatment of 5azaC or GA. These data were used to obtain genes upregulated in both 5azaC- orGA-treated H1299 cells.

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