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Post-slippage cells increase expression of factors associated with SASP.

ABSTRACT: Post-slippage cells increase expression of factors associated with SASP.

PROVIDER: PRJNA471655 | ENA |

REPOSITORIES: ENA

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Post-slippage cells increase expression of factors associated with SASP.

Project description:Human transcriptome analysis of U2OS cells treated with nocodazole or DMSO (Control). The gene expression profiling will reveal senescence-associated genes induced upon nocodazole treatment. Our preliminary data show that antimitotic drugs treatment promote post-slippage senescence.

2018-05-17 | GSE114515 | GEO

Unique human beta-cell senescence-associated secretory phenotype (SASP) reveal conserved signaling pathways and heterogeneous factors

Project description:The aging of pancreatic beta-cells may undermine their ability to compensate for insulin resistance, leading to the development of type 2 diabetes (T2D). Aging beta-cells acquire markers of cellular senescence and develop a senescence-associated secretory phenotype (SASP) that can lead to senescence and dysfunction of neighboring cells through paracrine actions, contributing to beta-cell failure. Herein, we defined the beta-cell SASP signature based on unbiased proteomic analysis of conditioned media of cells obtained from human senescent beta-cells. These experiments revealed that the beta-cell SASP is enriched for factors associated with inflammation, cellular stress response, and extracellular matrix remodeling across species.

2021-03-18 | GSE162521 | GEO

Effect of SASP factors on mouse intestinal organoids

Project description:Effect of SASP factors on mouse intestinal organoids

| PRJNA907085 | ENA

Mettl14-driven senescence-associated secretory phenotype (SASP) facilitates somatic reprogramming

Project description:The METTL3-METTL14 complex, as the "writer" of N6-methyladenosine (m6A), plays an important role in many biological processes. Previous studies have shown that overexpression of Mettl3 can increase the level of m6A and promotes somatic cell reprogramming. Here, we demonstrate that Mettl14, another component of the methyltransferase (MTase) complex, can significantly enhance the generation of induced pluripotent stem cells (iPSCs) in m6A independent manner. Cooperating with Oct4, Sox2, Klf4 and c-Myc (OSKM), Mettl14 transiently increased the senescence-associated secretory phenotype (SASP) gene expression in the non-reprogramming cells at the late reprogramming stage. The conditional medium in reprogramming intermediates overexpressing Mettl4 or its mutant could enhanced the reprogramming, so do IL-6, a component of SASP. Corespondingly, blocking of SASP using senolytic agent or NF-κB inhibitor impairs the effect of Mettl14 on reprogramming. . Our work highlights the m6A independent function of Mettl14 and provides new insight into the interplay between senescence and reprogramming in vitro.

2022-08-24 | GSE196475 | GEO

Unique human beta-cell senescence-associated secretory phenotype (SASP) reveal conserved signaling pathways and heterogeneous factors

Project description:Unique human beta-cell senescence-associated secretory phenotype (SASP) reveal conserved signaling pathways and heterogeneous factors

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Effect of SASP factors on mouse intestinal organoids [bulk RNA-seq]

Project description:Effect of SASP factors on mouse intestinal organoids [bulk RNA-seq]

| PRJNA907130 | ENA

Effect of SASP factors at single nucleus level of mouse intestinal organoids [snRNA-seq]

Project description:We report single nucleus RNAseq data from the mouse intestinal organoids cultured in quiescent or senescent conditioned media. Analysis revealed changes in cell composition and gene expression caused by SASP factors in senescent conditioned media.

2022-12-06 | GSE219127 | GEO

Mettl14-driven senescence-associated secretory phenotype (SASP) facilitates somatic reprogramming

Project description:Mettl14-driven senescence-associated secretory phenotype (SASP) facilitates somatic reprogramming

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Evaluation of the secretome of senescent melanoma cells and the impact of silencing Mfn1 on the senescence-associated secretory phenotype (SASP) by shotgun proteomics analysis.

Project description:Cellular senescence is a therapy endpoint in melanoma, and the senescence-associated secretory phenotype (SASP) can affect tumor growth and microenvironment, influencing treatment outcomes. Metabolic interventions can modulate the SASP, and an enhanced mitochondrial energy metabolism supports resistance to therapy in melanoma. In a previous report we showed that in melanoma, senescence induced by the DNA methylating agent temozolomide, increases fusion proteins mitofusins 1 and 2. Silencing Mfn1 or Mfn2 expression reduced interleukin-6 secretion by senescent cells. Here we expanded these observations evaluating the secretome of senescent melanoma cells using shotgun proteomics, and explored the impact of silencing Mfn1 on the SASP. A significant increase in proteins reported to reduce the immune response towards the tumor was found in the media of senescent cells. The secretion of several of these immunomodulatory proteins was affected by Mfn1 silencing, among them was galectin-9. In agreement, tumors lacking mitofusin 1 responded better to treatment with the methylating agent dacarbazine, tumor size was reduced and a higher immune cell infiltration was detected in the tumor. Our results highlight mitochondrial dynamic proteins as potential pharmacological targets to modulate the SASP in the context of melanoma treatment.

2024-01-26 | PXD043779 | Pride

Effect of SASP factors at single nucleus level of mouse intestinal organoids [snRNA-seq]

Project description:Effect of SASP factors at single nucleus level of mouse intestinal organoids [snRNA-seq]

| PRJNA907129 | ENA