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Chronic stress promotes intestinal stem cell aging [RNA-seq]

ABSTRACT: Chronic stress promotes intestinal stem cell aging [RNA-seq]

PROVIDER: PRJNA1090855 | ENA |

REPOSITORIES: ENA

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Chronic stress promotes intestinal stem cell aging

Project description:Chronic stress promotes intestinal stem cell aging

| PRJNA1090852 | ENA

Chronic stress promotes intestinal stem cell aging [scRNA-seq]

Project description:Chronic stress promotes intestinal stem cell aging [scRNA-seq]

| PRJNA1090857 | ENA

Chronic stress promotes intestinal stem cell aging [scRNA-seq]

Project description:To elucidate alterations in intestinal cell types under chronic stress, we conducted scRNA-seq analysis of intestinal crypts from NT and ES models. After that, we found that significant changes in ISCs in the ES group compared to the NT group. To validate the functional roles of ISCs, we performed RNA-seq of ISCs under different treatment conditions, we identified Chrm3-dependent differential genes between NT and ES groups, particularly noting downregulated genes associated with stemness and proliferation (e.g., Olfm4, Lgr5, and Mcm4), and upregulated genes linked to aging and calcium signaling pathways (e.g., Cdkn1a, Orai1, and Chp2), which contribute to ISC aging. These findings provided mechanistic insights into targeting these pathways to enhance intestinal function and integrity. Furthermore, to assess the impact of stress-induced changes in microbiota composition on ISC stemness, we synchronized microbiota between NT and ES groups through co-housing conditions and employed 16S rDNA sequencing. This analysis aimed to ascertain the possibility that changes in the microbiota composition whether contribute to the decline in ISC stemness under stress conditions. scRNA-seq of crypts were used to to characterize the diversity of cell lines under chronic stress. RNA-seq of ISC in Chrm3Lgr5+/+ and Chrm3Lgr5-/- mice from NT and ES mice were taken to delineate altered pathways and the mechanisms underlying ISC changes in ES model. 16S rDNA-seq (available in PRJNA1090629) were employed to confirm microbiota synchronization between NT and ES groups under co-housing conditions.

2025-02-08 | GSE262229 | GEO

Chronic stress promotes intestinal stem cell aging [RNA-seq]

Project description:To elucidate alterations in intestinal cell types under chronic stress, we conducted scRNA-seq analysis of intestinal crypts from NT and ES models. After that, we found that significant changes in ISCs in the ES group compared to the NT group. To validate the functional roles of ISCs, we performed RNA-seq of ISCs under different treatment conditions, we identified Chrm3-dependent differential genes between NT and ES groups, particularly noting downregulated genes associated with stemness and proliferation (e.g., Olfm4, Lgr5, and Mcm4), and upregulated genes linked to aging and calcium signaling pathways (e.g., Cdkn1a, Orai1, and Chp2), which contribute to ISC aging. These findings provided mechanistic insights into targeting these pathways to enhance intestinal function and integrity. Furthermore, to assess the impact of stress-induced changes in microbiota composition on ISC stemness, we synchronized microbiota between NT and ES groups through co-housing conditions and employed 16S rDNA sequencing. This analysis aimed to ascertain the possibility that changes in the microbiota composition whether contribute to the decline in ISC stemness under stress conditions. scRNA-seq of crypts were used to to characterize the diversity of cell lines under chronic stress. RNA-seq of ISC in Chrm3Lgr5+/+ and Chrm3Lgr5-/- mice from NT and ES mice were taken to delineate altered pathways and the mechanisms underlying ISC changes in ES model. 16S rDNA-seq were employed to confirm microbiota synchronization between NT and ES groups under co-housing conditions.

2025-02-08 | GSE262228 | GEO

Aging Promotes Metabolic Dysfunction-associated Steatotic Liver Disease and Multi-Organ Dysfunction by Inducing Ferroptotic Stress

Project description:Aging is an inevitable consequence of living that undermines cellular resiliency to cause tissue degeneration and eventual multi-organ dysfunction. Susceptibility to biological consequences of aging varies among organs and individuals. Stressors that challenge resiliency unmask these differences. Hence, aging increases the risk for failure of many metabolically-stressed organs and exacerbates liver degeneration related to obesity and diabetes. We discovered that aging promotes ferroptosis, a type of metabolism-regulated cell death, in hepatocytes. Hepatocytes that have launched the ferroptotic death program adapt their metabolism to survive but become damaged and dysfunctional. Metabolic stressors amplify this, increasing the burden of ferroptosis-adapted cells and liver damage. Blocking ferroptotic signaling in old livers reduces accumulation of adapted hepatocytes and reverts livers to a more youthful resilient state despite exogenous stressors. Ferroptosis is also induced in other organs that are damaged by chronic metabolic stress, identifying ferroptosis as a tractable conserved mechanism for aging-related multi-organ dysfunction.

2024-07-01 | GSE262457 | GEO

Astrocytic CREB in nucleus accumbens promotes susceptibility to chronic stress

Project description:Astrocytic CREB in nucleus accumbens promotes susceptibility to chronic stress

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Chronic stress promotes intestinal stem cell aging

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-02-08 | GSE262230 | GEO

Chronic restraint stress increases transcriptomic indicators of biological aging in mouse bone marrow leukocytes

Project description:Genome-wide transcriptional profiling results were used to examine the effect of a psychological stress paradigm for rodents (chronic restraint) on indicies of biological aging in murine femoral bone marrow leukocytes and to assess the extent to which propranolol could block such effects.

2021-03-31 | GSE157133 | GEO

Molecular chaperone Hsp90 supports adaptive cell size increase in response to chronic stress

Project description:Hsf1, well known for its role in acute stress responses, is required for the cell size increase, and that the molecular chaperone Hsp90 is essential for coupling the cell size increase to augmented translation through a translational "rewiring stress response". We propose that this protective process of chronic stress adaptation contributes to the increase in size as cells get older, and that its failure promotes aging.

2023-12-01 | PXD039672 | Pride

Aging Promotes Metabolic Dysfunction-Associated Steatotic Liver Disease by Inducing Ferroptotic Stress

Project description:Aging Promotes Metabolic Dysfunction-Associated Steatotic Liver Disease by Inducing Ferroptotic Stress

| PRJNA1094958 | ENA