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Impaired immune surveillance accelerates accumulation of senescent cells and aging [RNA-seq]

ABSTRACT: Impaired immune surveillance accelerates accumulation of senescent cells and aging [RNA-seq]

PROVIDER: PRJNA474833 | ENA |

REPOSITORIES: ENA

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Impaired immune surveillance accelerates accumulation of senescent cells and aging [RNA-seq]

Project description:Cellular senescence is a stress response that imposes stable cell-cycle arrest in damaged cells, preventing their propagation in tissues. However, long-term presence of senescent cells might promote tissue degeneration and malignant transformation via secreted pro-inflammatory and matrix-remodeling factors. These factors lead to immune-cell recruitment and senescent-cell clearance. Senescent cells accumulate in tissues in advanced age. The extent of immune-system involvement in regulating age-related accumulation of senescent cells, and its consequences, are unknown. Here we show that mice with impaired cell cytotoxicity exhibit both higher senescent-cell tissue burden and chronic inflammation. They suffer from multiple age-related disorders and significantly lower survival. Strikingly, pharmacological elimination of senescent-cells by ABT-737 partially alleviates accelerated aging phenotype in these mice. In progeroid mice, impaired cell cytotoxicity further promotes senescent-cell accumulation and shortens lifespan. ABT-737 administration during the second half of life of these progeroid mice abrogates senescence signature and increases median survival. Our findings shed new light on mechanisms governing senescent-cell presence in aging, and could motivate new strategies for regenerative medicine.

2018-11-20 | GSE115401 | GEO

Impaired immune surveillance accelerates accumulation of senescent cells and aging.

Project description: Not available

| S-EPMC6303397 | biostudies-literature

Transcriptomic profiling of human senescent cells upon treatment with the senolytic agent procyanidin C1

Project description:In the course of aging, the long term retention of senescent cells in vivo, a process mainly attributed to highly expressed BCL-family proteins, chronically damages tissues mainly through a senescence-associated secretory phenotype (SASP). It has been documented that accumulation of senescent cells accelerates aging and contributes to age-related diseases. Indeed, senescent cells can be removed by several strategies, thus preventing occurrence of chronic disorders and prolonging lifespan and healthspan. Senolytics, which eliminate senescent cells by pharmacological intervention, have recently emerged as a new line of therapeutic agents to ameliorate diverse age-related pathologies. Achieving the goal using natural or synthetic agents would have a tremendous impact on the quality of life. We report the potential of procyanidin C1 (PCC1), an epicatechin trimer natural product derived from plant sources including grape, apple, and cocoa, in targeting senescent cells via induction of apoptosis. This study demonstrates the efficacy of PCC1 in minimizing the influence of senescent cells in tissue microenvironment and provides a strong rationale for its future use in aging control and geriatric medicine.

2021-10-04 | GSE164012 | GEO

Targeted Apoptosis of Senescent Cells Restores Tissue Homeostasis in Response to Chemotoxicity and Aging

Project description:The accumulation of irreparable cellular damage restricts healthy lifespan after acute stress or natural aging. Senescent cells are thought to impair tissue function and their genetic clearance can successfully delay features of aging. Identifying how senescent cells avoid apoptosis would allow for the prospective design of anti-senescence compounds to address whether homeostasis can be restored. Here, we identify FOXO4 as a pivot in the maintenance of senescent cell viability. We designed a FOXO4-based peptide which selectively competes for interaction of FOXO4 with p53. In senescent cells, this results in p53 nuclear exclusion and cell-intrinsic apoptosis. Importantly, under conditions where it was well tolerated, the FOXO4 peptide restored liver function after Doxorubicin-induced chemotoxicity. Moreover, in fast aging XpdTTD/TTD, as well as in naturally aged mice the FOXO4 peptide could counteract the loss of fitness, fur density and renal function. Thus, it is possible to therapeutically target senescent cells and thereby effectively counteract senescence-associated loss of tissue homeostasis.

2017-03-01 | GSE94395 | GEO

Phytosterol accumulation results in ventricular arrhythmia, impaired cardiac function and death

Project description:Phytosterol accumulation results in ventricular arrhythmia, impaired cardiac function and death

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Genome wide mapping of gH2AX in quiescent and irradiation-induced senescent human fibroblasts

Project description:We observe preferential accumulation of gH2AX at chromosome ends upon irradiation comparison of quiescent vs senescent human fibroblasts

2012-03-13 | E-GEOD-35884 | biostudies-arrayexpress

Impaired efferocytosis enables apoptotic osteoblasts to escape osteoimmune surveillance during aging

Project description:Impaired efferocytosis enables apoptotic osteoblasts to escape osteoimmune surveillance during aging

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Musashi 2 regulates normal hematopoiesis and accelerates leukemogenesis

Project description:This SuperSeries is composed of the following subset Series: GSE16432: MSI2 regulates hematopoiesis and accelerates leukemogenesis GSE22773: Musashi 2 regulates normal hematopoiesis and accelerates leukemogenesis (LK and MS12-inducible) GSE22774: Musashi 2 regulates normal hematopoiesis and accelerates leukemogenesis (LSK and LK) GSE22775: Musashi 2 regulates normal hematopoiesis and accelerates leukemogenesis (Leukemia cell lines) Refer to individual Series

2010-07-21 | E-GEOD-22778 | biostudies-arrayexpress

Impaired efferocytosis enables apoptotic osteoblasts to escape osteoimmune surveillance during aging (mRNA)

Project description:Impaired efferocytosis enables apoptotic osteoblasts to escape osteoimmune surveillance during aging (mRNA)

| PRJNA832555 | ENA

Impaired efferocytosis enables apoptotic osteoblasts to escape osteoimmune surveillance during aging (miRNA)

Project description:Impaired efferocytosis enables apoptotic osteoblasts to escape osteoimmune surveillance during aging (miRNA)

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