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Architectural alterations in enhancer repertoires orchestrate senescence-associated secretory phenotype profile

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE117210 | GEO | 2018/07/18

REPOSITORIES: GEO

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Architectural alterations in enhancer repertoires orchestrate senescence-associated secretory phenotype profile [Hi-C]

Project description:The emerging 4D genome project aiming to map the dynamics of genomes in spatial and temporal dimension has put forward to developing the mechanisms of how the nucleus is organized and functions. Therefore, processes like cellular senescence characterized by complex events give rise to understanding the regulation network from 1D genome to dynamically organized 3D structure. Unfortunately, how spatial genome reorganization triggers cellular senescence and how it influences senescence-related downstream transcriptional profile remains unaddressed well. Here, we uncover that re re-orchestration of 3D chromatin architecture has occurred in cellular senescence, accompanied with remodeling of enhancer repertories, which in turn facilicate the recruitment of the chromatin reader C/EBPα to newly activated senescence enhancers (SAEs), leading to the expression of SAEs flanking SASP genes kinetics.

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Architectural alterations in enhancer repertoires orchestrate senescence-associated secretory phenotype profile [ChIP-seq]

2018-07-18 | GSE117209 | GEO

Architectural alterations in enhancer repertoires orchestrate senescence-associated secretory phenotype profile [RNA-seq]

2018-07-18 | GSE117208 | GEO

Architectural alterations in enhancer repertoires orchestrate senescence-associated secretory phenotype profile

Project description:Architectural alterations in enhancer repertoires orchestrate senescence-associated secretory phenotype profile

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Architectural alterations in enhancer repertoires orchestrate senescence-associated secretory phenotype profile [RNA-seq]

Project description:Architectural alterations in enhancer repertoires orchestrate senescence-associated secretory phenotype profile [RNA-seq]

| PRJNA481465 | ENA

Architectural alterations in enhancer repertoires orchestrate senescence-associated secretory phenotype profile [ChIP-seq]

Project description:Architectural alterations in enhancer repertoires orchestrate senescence-associated secretory phenotype profile [ChIP-seq]

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Architectural alterations in enhancer repertoires orchestrate senescence-associated secretory phenotype profile [Hi-C]

Project description:Architectural alterations in enhancer repertoires orchestrate senescence-associated secretory phenotype profile [Hi-C]

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Senescence-activated enhancer landscape orchestrates the senescence-associated secretory phenotype in murine fibroblasts.

Project description:The three-dimensional configuration of the chromatin architecture is known to be crucial for alterations in the transcriptional network; however, the underlying mechanisms of epigenetic control of senescence-related gene expression by modulating the chromatin architecture remain unknown. Here, we demonstrate frequent chromosomal compartment switching during mouse embryonic fibroblasts (MEFs) replicative senescence as characterized by senescence-inactivated (SIAEs) and -activated enhancers (SAEs) in topologically associated domains (TADs). Mechanistically, SAEs are closely correlated with senescence-associated secretory phenotype (SASP) genes, which are a key transcriptional feature of an aging microenvironment that contributes to tumor progression, aging acceleration, and immunoinflammatory responses. Moreover, SAEs can positively regulate robust changes in SASP expression. The transcription factor CCAAT/enhancer binding protein α (C/EBPα) is capable of enhancing SAE activity, which accelerates the emergence of SAEs flanking SASPs and the secretion of downstream factors, contributing to the progression of senescence. Our results provide novel insight into the TAD-related control of SASP gene expression by revealing hierarchical roles of the chromatin architecture, transcription factors, and enhancer activity in the regulation of cellular senescence.

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Senescence associated secretory phenotype profile from primary lung mice fibroblasts depends on the senescence induction stimuli.

Project description:Cellular senescence is a multifactorial phenomenon of growth arrest and distorted function, which has been recognized as an important feature during tumor suppression mechanisms and a contributor to aging. Senescent cells have an altered secretion pattern called Senescence-Associated Secretory Phenotype (SASP) that comprises a complex mix of factors including cytokines, growth factors, chemokines, and matrix metalloproteinases. SASP has been related with local inflammation that leads to cellular transformation and neurodegenerative diseases. Various pathways for senescence induction have been proposed; the most studied is replicative senescence due to telomere attrition called replicative senescence (RS). However, senescence can be prematurely achieved when cells are exposed to diverse stimuli such as oxidative stress (stress-induced premature senescence, SIPS) or proteasome inhibition (proteasome inhibition-induced premature senescence, PIIPS). SASP has been characterized in RS and SIPS but not in PIIPS. Hence, our aim was to determine SASP components in primary lung fibroblasts obtained from CD-1 mice induced to senescence by PIIPS and compare them to RS and SIPS. Our results showed important variations in the 62 cytokines analyzed, while SIPS and RS showed an increase in the secretion of most cytokines, and in PIIPS only 13 were incremented. Variations in glutathione-redox balance were also observed in SIPS and RS, and not in PIIPS. All senescence types SASP displayed a pro-inflammatory profile and increased proliferation in L929 mice fibroblasts exposed to SASP. However, the behavior observed was not exactly the same, suggesting that the senescence induction pathway might encompass dissimilar responses in adjacent cells and promote different outcomes.

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Iron accumulation drives fibrosis, senescence and the senescence-associated secretory phenotype.

Project description:Fibrogenesis is part of a normal protective response to tissue injury that can become irreversible and progressive, leading to fatal diseases. Senescent cells are a main driver of fibrotic diseases through their secretome, known as senescence-associated secretory phenotype (SASP). Here, we report that cellular senescence, and multiple types of fibrotic diseases in mice and humans are characterized by the accumulation of iron. We show that vascular and hemolytic injuries are efficient in triggering iron accumulation, which in turn can cause senescence and promote fibrosis. Notably, we find that senescent cells persistently accumulate iron, even when the surge of extracellular iron has subdued. Indeed, under normal conditions of extracellular iron, cells exposed to different types of senescence-inducing insults accumulate abundant ferritin-bound iron, mostly within lysosomes, and present high levels of labile iron, which fuels the generation of reactive oxygen species and the SASP. Finally, we demonstrate that detection of iron by magnetic resonance imaging might allow non-invasive assessment of fibrotic burden in the kidneys of mice and in patients with renal fibrosis. Our findings suggest that iron accumulation plays a central role in senescence and fibrosis, even when the initiating events may be independent of iron, and identify iron metabolism as a potential therapeutic target for senescence-associated diseases.

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