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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE219127 | GEO | 2022/12/06

REPOSITORIES: GEO

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SASP signature of beta-cells includes pro-inflammatory and stress response proteins

Project description:To define the senescence-associated secretory phenotype (SASP) of beta-cells, we used conditioned media (CM) generated from bleomycin-treated MIN6 cells and from senescent (beta-Gal-positive) primary beta-cells. In order to culture senescent beta-cells, we isolated islet, FACS-sorted them into beta-Gal-positive and negative populations, excluding immune cells through negative selection of CD45-positive and CD11beta-positive cells. For both the MIN6 and primary beta-cell models, we cultured cells in serum-free media to generate CM for proteomic analysis using the aptamer-based SomaScan platform.

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

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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]

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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.

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