Single cell transcriptomes of replicatively cellular senescenct cells and ionizing radiation induced senescent cells
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE119807 | GEO | 2018/11/19
REPOSITORIES: GEO
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Project description:Microarrays analysis identifies WNT16in senescent fibroblasts. To identify genes expressed in replicative senescence, microarray experiments were conducted in which we compared the RNA expression profile of young MRC5 fibroblasts at population doubling 28 (PDL28) and replicative senescent MRC5 fibroblasts at PDL63. In total, 177 gene probes were upregulated and 338 gene probes were downregulated in senescent versus young MRC5 fibroblasts. Genes were classified based on mapping to KEGG pathways. Upregulated genes were enriched in three KEGG pathways, the Wingless-type MMTV integration site (WNT) signaling pathway (WNT16, PLCB4, CCND2, SFRP1, WNT5B, RAC2), cytokine-cytokine receptor interaction (TNFRSF10D, TNFRSF10B, TNFRSF10C, IL1R2, IL18, VEGFC), and the p53 signaling pathway (CDKN1A, TNFRSF10B, PERP, STEAP3, ZMAT3). Repressed genes were enriched in three KEGG pathways, cell cycle (PKMYT1, CDC7, CCNE2, MCM4, BUB1, CDC25A, CDKN1B, MCM6, PLK1, CDKN2C, CCNB2, MCM3, BUB1B, CCNA2, CDC2), cytokine-cytokine receptor interaction (KITLG, IL11, TNFSF4, CCL2, PDGFRA, TNFRSF11B, TGFBR1, IL1R1, TNFRSF19), and DNA replication (POLE, RFC2, MCM4, RNASEH2B, POLA1, DNA2, MCM6, PRIM1, RFC4, MCM3). Along with p53 transcriptional targets (CDKN1A, PERP, WIG1), genes encoding secreted factors (WNT16, MMP10, MMP3) were among the most strongly increased in senescent cells. Six arrays were hybridized with complex probes consisting of RNA isolated from MRC5 fibroblasts at population doubling 63 (undergoing replicative senescence) and RNA isolated from MRC5 fibroblats at population doubling 28 (young). The six arrays correspond to three biological replicates, each with a dye-swap technical replicate.
2010-05-18 | E-GEOD-15919 | biostudies-arrayexpress
Project description:Microarrays analysis identifies WNT16in senescent fibroblasts. To identify genes expressed in replicative senescence, microarray experiments were conducted in which we compared the RNA expression profile of young MRC5 fibroblasts at population doubling 28 (PDL28) and replicative senescent MRC5 fibroblasts at PDL63. In total, 177 gene probes were upregulated and 338 gene probes were downregulated in senescent versus young MRC5 fibroblasts. Genes were classified based on mapping to KEGG pathways. Upregulated genes were enriched in three KEGG pathways, the Wingless-type MMTV integration site (WNT) signaling pathway (WNT16, PLCB4, CCND2, SFRP1, WNT5B, RAC2), cytokine-cytokine receptor interaction (TNFRSF10D, TNFRSF10B, TNFRSF10C, IL1R2, IL18, VEGFC), and the p53 signaling pathway (CDKN1A, TNFRSF10B, PERP, STEAP3, ZMAT3). Repressed genes were enriched in three KEGG pathways, cell cycle (PKMYT1, CDC7, CCNE2, MCM4, BUB1, CDC25A, CDKN1B, MCM6, PLK1, CDKN2C, CCNB2, MCM3, BUB1B, CCNA2, CDC2), cytokine-cytokine receptor interaction (KITLG, IL11, TNFSF4, CCL2, PDGFRA, TNFRSF11B, TGFBR1, IL1R1, TNFRSF19), and DNA replication (POLE, RFC2, MCM4, RNASEH2B, POLA1, DNA2, MCM6, PRIM1, RFC4, MCM3). Along with p53 transcriptional targets (CDKN1A, PERP, WIG1), genes encoding secreted factors (WNT16, MMP10, MMP3) were among the most strongly increased in senescent cells.
2009-12-15 | GSE15919 | GEO
Project description:Altered DNA methylation and associated destabilization of genome integrity and function is a hallmark of cancer. Replicative senescence imposes a limit on proliferative potential that all cancer cells must bypass. Compared to proliferating cells, senescent cells exhibit marked chromatin re-organization. Here we show by whole-genome single-nucleotide bisulfite sequencing that replicative senescent human cells exhibit widespread alterations in their DNA methylome. These changes are linked to mislocalization of the maintenance DNA methyltransferase (DNMT1) in cells approaching senescence, altered replication-coupled DNA methylation and de-repression of repetitive satellite sequences. Deficiency of DNMT1 triggers chromatin changes characteristic of senescence and expression of satellite sequences. Most importantly, but paradoxically, gains and losses of methylation in replicative senescence are similar to those in cancer, and this M-bM-^@M-^XreprogrammedM-bM-^@M-^Y methylation landscape is largely retained when cells escape or bypass senescence. In sum, altered regulation of DNMT1 in cells approaching replicative senescence contributes to changes in chromatin structure and function. Consequently, if senescent cells escape the proliferative barrier, they already harbor epigenetic changes likely to promote malignancy. Examination of methylation status in IMR90 cells
2013-11-25 | E-GEOD-48580 | biostudies-arrayexpress
Project description:Purpose: Use RNA-seq strategy to characterize the PD-L1 correlated genes in sorted PD-L1 negative and positive doxorubicin-induced senescent and normal human foreskin fibroblasts HCA2 cells to identify the upstream transcriptional network for regulating heterogeneous PD-L1 expression in senescent cells. Methods: Early passaged normal HCA2 cells and senescent HCA2 cells induced by 24 hours of 100 nM doxorubicin treatment were utilized for the preparation of bulk RNA-seq libraries. Among the senescent cells, PD-L1 positive and negative cells were separated by FACSorting.
2022-08-27 | GSE198396 | GEO
Project description:Altered DNA methylation and associated destabilization of genome integrity and function is a hallmark of cancer. Replicative senescence imposes a limit on proliferative potential that all cancer cells must bypass. Compared to proliferating cells, senescent cells exhibit marked chromatin re-organization. Here we show by whole-genome single-nucleotide bisulfite sequencing that replicative senescent human cells exhibit widespread alterations in their DNA methylome. These changes are linked to mislocalization of the maintenance DNA methyltransferase (DNMT1) in cells approaching senescence, altered replication-coupled DNA methylation and de-repression of repetitive satellite sequences. Deficiency of DNMT1 triggers chromatin changes characteristic of senescence and expression of satellite sequences. Most importantly, but paradoxically, gains and losses of methylation in replicative senescence are similar to those in cancer, and this ‘reprogrammed’ methylation landscape is largely retained when cells escape or bypass senescence. In sum, altered regulation of DNMT1 in cells approaching replicative senescence contributes to changes in chromatin structure and function. Consequently, if senescent cells escape the proliferative barrier, they already harbor epigenetic changes likely to promote malignancy.
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Project description:Senescent cells secrete many molecules, which contribute to the prevention of cancer progression. We induced MSC senescence by oxidative stress, DNA damage, and replicative exhaustion. The first two are considered inducers of acute senescence while extensive proliferation triggers replicative senescence also named chronic senescence. We cultivated cancer cells in the presence of acute and chronic senescent MSC conditioned media and evaluated proliferation, DNA damage, apoptosis and senescence.
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Project description:MicroRNAs regulate various cellular processes. While several genes associated with replicative senescence have been described in endothelial cells, miRNAs that regulate these genes remain largely unknown. The present study was designed to identify miRNAs associated with replicative senescence and their target genes in HUVECs. We have employed Agilent Human MicroRNAs microarray platform to evaluate the expressions of 866 human miRNAs and 89 human viral miRNAs, based on Sanger miRNA database release 12.0 miRNA expression profiles were established for young and replicative senescent HUVECs
2013-04-05 | E-GEOD-37092 | biostudies-arrayexpress
Project description:The accumulation of senescent cells promotes aging, but a molecular mechanism that senescent cells use to evade immune clearance and accumulate remains to be elucidated. Here, we report that p16-positive senescent cells upregulate the immune checkpoint protein programmed death-ligand 1 (PD-L1) to accumulate in aging and chronic inflammation. p16-mediated inhibition of CDK4/6 promotes PD-L1 stability in senescent cells via the downregulation of ubiquitin-dependent degradation. p16 expression in infiltrating macrophages induces an immunosuppressive environment that can contribute to an increased burden of senescent cells. Treatment with immunostimulatory anti-PD-L1 antibody enhances the cytotoxic T cell activity and leads to the elimination of p16, PD-L1-positive cells. Our study uncovers a molecular mechanism of p16-dependent regulation of PD-L1 protein stability in senescent cells and reveals the potential of PD-L1 as a target for treating senescence-mediated age-associated diseases.
2024-02-14 | GSE225286 | GEO
Project description:The accumulation of senescent cells promotes aging, but a molecular mechanism that senescent cells use to evade immune clearance and accumulate remains to be elucidated. Here, we report that p16-positive senescent cells upregulate the immune checkpoint protein programmed death-ligand 1 (PD-L1) to accumulate in aging and chronic inflammation. p16-mediated inhibition of CDK4/6 promotes PD-L1 stability in senescent cells via the downregulation of ubiquitin-dependent degradation. p16 expression in infiltrating macrophages induces an immunosuppressive environment that can contribute to an increased burden of senescent cells. Treatment with immunostimulatory anti-PD-L1 antibody enhances the cytotoxic T cell activity and leads to the elimination of p16, PD-L1-positive cells. Our study uncovers a molecular mechanism of p16-dependent regulation of PD-L1 protein stability in senescent cells and reveals the potential of PD-L1 as a target for treating senescence-mediated age-associated diseases.
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