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The effect of senescent cells depletion in obese hearts

ABSTRACT: The effect of senescent cells depletion in obese hearts

PROVIDER: PRJNA1101952 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28735752_1.fastq.gz	Fastqsanger.gz
	SRR28735752_2.fastq.gz	Fastqsanger.gz
	SRR28735753_1.fastq.gz	Fastqsanger.gz
	SRR28735753_2.fastq.gz	Fastqsanger.gz
	SRR28735755_1.fastq.gz	Fastqsanger.gz

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The effect of senescent cells depletion in obese hearts

Project description:Obesity is a major contributor to metabolic and cardiovascular diseases. Senescence is a highly dynamic process activated by diverse stimuli and increased cellular senescence has been associated with age-related disorders. Here, we investigated the impact of cellular senescence in obesogenic diet-related metabolic and cardiac dysfunctions. An obesogenic diet induced an increase on body weight gain and adiposity, glucose intolerance, insulin resistance, dyslipidemia, and hepatic disorders in mice; however, these alterations were prevented by a senolytic cocktail (dasatinib and quercetin), which leads to removal of senescent cells. In addition, the elimination of senescent cells counteracted the activation of the senescent program and DNA damage in the white adipose tissue (WAT) induced by an obesogenic diet. Obese mice had an increase of the senescence-associated secretory phenotype (SASP) and DNA damage in the heart, cardiac hypertrophy, and diastolic dysfunction; however, the use of a senolytic combination abolished these myocardial alterations caused by an obesogenic diet. Transcriptomic analysis of the hearts revealed that obese mice exhibited a downregulation of genes associated with fatty acid metabolism, oxidative phosphorylation, PI3K AKT MTOR signaling, P53 pathway, and DNA repair; however, the treatment with senolytic cocktail induced an increase of these pathways in the heart. Collectively, these data suggest that obesogenic diet elicits WAT and cardiac senescence program in mice, and that targeting senescent cells may be a novel therapeutic strategy for attenuating obesity-related metabolic and cardiac disorders.

2024-12-19 | GSE264313 | GEO

Oenothera effect on senescent NDHF

Project description:Accumulation of senescent dermal fibroblasts drives skin aging, impairing the integrity of the extracellular matrix (ECM) and the function of neighbouring cells. One of strategies to manipulate cell senescence include the reactivation of proliferation. Here, a data independent mass spectrometry based proteomic approach has been used to evaluate the effect of an hydrophilic Oenothera biennis cell culture extract (ObHEx) on senescent human dermal fibroblasts. It has been shown that the extract was able to affect the levels of 18 proteins which cluster together and point to mitosis pathways. Indeed the treatment with ObHEx increase the expression of CDK1, replicative helicase complex (MCM2, MCM3, MCM4, MCM5, MCM6, MCM7), condensin I complex (NCAPD2, NCAPH, NCAPG, SMC4, SMC2) and other proteins related to kinetochore (KNTC1, NUF2, TRIP13). This strongly suggests that ObHEx could restore the proliferation of senescent fibroblasts.

2023-03-10 | PXD034222 | Pride

Transcription profiling of human BRAFE600-expressing, senescent fibroblast cells that have bypassed oncogene-induced senescence by depletion of C/EBPb a

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Effect of depletion of pre-existing senescent cells in aged hamstrers on gene expression in lungs

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Effect of depletion of C10orf71 on gene expression in hearts from embryonic mice at E18.5 and adult mice

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Podocytes from Hypertensive and Obese Mice Acquire an Inflammatory, Senescent and Aged Phenotype

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Senescent cancer-associated fibroblasts in pancreatic adenocarcinoma impair CD8+ T cell activation and limit responsiveness to immunotherapy in mice

Project description:Senescent cells within tumors and their stroma exert complex pro- and anti-tumorigenic functions, yet the potential for targeting such senescent cells for improved therapy remains largely unknown. Here, we uncover the presence of a senescent subset of cancer-associated fibroblasts (CAFs) within pancreatic ductal adenocarcinomas (PDAC) and in premalignant lesions in mice and humans. Senescent CAFs represented different previously-defined CAF subtypes. Senescent CAFs isolated from mouse and humans expressed elevated levels of immunoregulatory genes. Depletion of senescent CAFs, either genetically or using the Bcl-2 inhibitor ABT-199 (venetoclax), increased the proportion of activated CD8+ T cells in mouse pancreatic carcinomas, whereas induction of CAF senescence had the opposite effect. Combining ABT-199 with an immune checkpoint therapy regimen significantly reduced mouse tumor burden. These results indicate that senescent CAFs in PDAC stroma limit the numbers of activated cytotoxic CD8+ T cells, and suggest that their targeted elimination through senolytic treatment may enhance immunotherapy.

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