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Suppression of inflammaging prolongs hematopoietic healthspan [dataset 3]

ABSTRACT: The impact of Thbs1 gene deletion on HSC activity during physiological aging is unknown. In this experiment, RNA Seq analysis was performed on BM HSCs derived from aged (18 month-old) Thbs1 knockout mice. HSCs derived from young (3 month-old) and aged (18 month-old) control mice were used as controls for comparison.

ORGANISM(S): Mus musculus

PROVIDER: GSE255652 | GEO | 2025/01/03

REPOSITORIES: GEO

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Suppression of inflammaging prolongs hematopoietic healthspan [dataset 5]

Project description:The impact of Thbs1 gene deletion on BMEC activity during physiological aging is unknown. In this experiment, RNA Seq analysis was performed on BMECs derived from aged (18 month-old) Thbs1 knockout mice. BMECs derived from young (3 month-old) and aged (18 month-old) control mice were used as controls for comparison.

2025-01-03 | GSE255654 | GEO

Suppression of inflammaging prolongs hematopoietic healthspan [dataset 4]

Project description:The impact of Thbs1 gene deletion on BM MSC activity during physiological aging is unknown. In this experiment, RNA Seq analysis was performed on BM MSCs derived from aged (18 month-old) Thbs1 knockout mice. MSCs derived from young (3 month-old) and aged (18 month-old) control mice were used as controls for comparison.

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Suppression of inflammaging prolongs hematopoietic healthspan [dataset 1]

Project description:The impact of Thbs1 gene deletion on HSC activity in vivo is unexplored. In this experiment, RNA Seq analysis was performed on BM HSCs derived from young (4 month-old) control and Thbs1 knockout mice to characterize transcriptional alterations resulting from constitutive deletion of Thbs1.

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Suppression of inflammaging prolongs hematopoietic healthspan [dataset 2]

Project description:The impact of recombinant Thbs1 (rThbs1) on HSC activity is unknown. In this experiment, RNA Seq analysis was performed on BM HSCs derived from young (4 month-old) control mice that were cultured ex vivo for 11 days in the presence or absence of rThbs1 (500 ng/mL). Additionally, RNA Seq analysis of HSCs cultured with rThbs1 in the presence of its neutralizing antibody (Clone A4.1) or its isotype control was performed to identify the pathways that are altered in HSCs upon exposure to rThbs1.

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Suppression of inflammaging prolongs hematopoietic healthspan.

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

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Restoring bone marrow niche function rejuvenates aged hematopoietic stem cells by reactivating the DNA Damage Response [4]

Project description:The bone marrow (BM) niche comprised of BM endothelial cells (BMECs) and LepR+ mesenchymal stromal cells (MSCs), plays a critical role in preserving the fitness of hematopoietic stem cells (HSCs). Aging is associated with defects in the BM niche that impair their ability to support HSC activity. However, mechanisms underlying age-related defects in the BM niche remain poorly understood. In this study, we identify BM niche derived Netrin-1 (NTN1) as a critical regulator of BM niche cell fitness during aging. Conditional deletion of NTN-1 specifically within BM MSCs or BMECs of young mice resulted in premature aging phenotypes within the BM niche including increased vascular leakiness, hypoxia, DNA damage and adiposity. On the other hand, supplementation of aged mice with NTN1 resulted in restoration of these hallmark niche defects and a rejuvenation of HSC activity. Mechanistically, we identify NTN1 as a critical regulator of DNA Damage Response (DDR) within BM niche cells and HSCs. In this experiment, RNA Seq analysis was performed on HSCs derived from young mice (3 month old), PBS treated aged mice (18 month old), and NTN1 treated aged mice (18 month old), to characterize transcriptional alterations within HSCs during aging, and following NTN1 treatment of aged mice.

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