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Global landscape mapping of chromatin accessibility in DNA damage-induced senescent human stromal cells

ABSTRACT: Global landscape mapping of chromatin accessibility in DNA damage-induced senescent human stromal cells

PROVIDER: PRJNA559076 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9915540_1.fastq.gz	Fastqsanger.gz
	SRR9915540_2.fastq.gz	Fastqsanger.gz
	SRR9915532_1.fastq.gz	Fastqsanger.gz
	SRR9915532_2.fastq.gz	Fastqsanger.gz
	SRR9915533_1.fastq.gz	Fastqsanger.gz

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Global landscape mapping of chromatin accessibility in DNA damage-induced senescent human stromal cells

Project description:We report the application of an improved assay for transposase-accessible chromatin with high-throughput sequencing in profiling changes of chromatin openning state in senescent human stromal cells. By obtaining over four billion bases of sequence from Tn5 transposase-processed chromosome DNAs, we generated genome-wide chromatin-state maps of human primary stromal cells (with a starting cell number of 50,000). This study provides a framework for the application of ATAC-Seq technique towards spatiotemporal chromatin configuration of human stromal cells upon DNA damage-induced senescence.

2021-03-23 | GSE135481 | GEO

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Project description:Global landscape mapping of chromatin accessibility in therapy-induced senescent human stromal cells

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Global landscape mapping of chromatin accessibility in therapy-induced senescent human stromal cells

Project description:We report the application of an improved assay for transposase-accessible chromatin with high-throughput sequencing in profiling changes of chromatin openning status in senescent human stromal cells. By obtaining over four billion bases of sequence from Tn5 transposase-processed chromosome DNAs, we generated genome-wide chromatin-state maps of human primary prostate stromal cells (with a starting cell number of 50,000). This study provides a framework for the application of ATAC-Seq technique towards spatiotemporal chromatin configuration of human stromal cells upon therapy-induced senescence, which is usually caused by typical DDR in damaged cells.

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Accumulating DNA damage and insufficient DNA repair in senescent cells underlie persistent DNA damage signaling

Project description:Senescent cells are a major cause of organismal aging and a key target for anti-aging therapies. Persistent DNA damage signaling is a primary driver of the induction and maintenance of cellular senescence. However, many DNA damaging stimuli that induce senescence, such as irradiation or transient exposure to genotoxic drugs, are transient. The mechanisms underlying persistent damage signaling in senescent cells, and why senescent cells fail to repair damaged DNA, remain unknown. Here, we were able to assess the mechanisms underlying persistence of DNA damage and senescence maintenance by designing a precisely controllable senescence system that does not require potent stressors to induce senescence. We demonstrate that sustained mTORC1 signaling in senescent cells causes gradually accumulating DNA damage and an inflammatory response that maintains cell-cycle arrest. Markedly, activation of E2F transcription, which promotes expression of DNA repair proteins, can reverse accumulated DNA damage. Thus, persistent DNA damage signaling arises in senescent cells by uncoupling of mTORC1 and E2F signaling, whereby prolonged mTORC1 activity causes gradually increasing DNA damage that cannot be sufficiently repaired without induction of protective E2F target genes.

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Project description:Alterations in the tissue microenvironment collaborate with cell autonomous genetic changes to contribute to neoplastic progression. The importance of the microenvironment in neoplastic progression is underscored by studies demonstrating that fibroblasts isolated from a tumor stimulate the growth of preneoplastic and neoplastic cells in xenograft models. Similarly, senescent fibroblasts promote preneoplastic cell growth in vitro and in vivo. Because senescent cells accumulate with age, their presence is hypothesized to facilitate preneoplastic cell growth and tumor formation in older individuals. To identify senescent stromal factors directly responsible for stimulating preneoplastic cell growth, we carried out whole genome transcriptional profiling and compared senescent fibroblasts to their younger counterparts. We identified osteopontin (OPN) as one of the most highly elevated transcripts in senescent fibroblasts. Importantly, reduction of OPN protein levels by RNAi did not impact senescence induction in fibroblasts; however, it dramatically reduced the growth-promoting activities of senescent fibroblasts in vitro and in vivo, demonstrating that OPN is necessary for paracrine stimulation of preneoplastic cell growth. In addition, we found that recombinant OPN was sufficient to stimulate preneoplastic cell growth. Finally, we demonstrate that OPN is expressed in senescent stroma within preneoplastic lesions that arise following DMBA/TPA treatment of mice, suggesting that stromal-derived OPN-mediated signaling events impact neoplastic progression.

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