IMR90 Senescence
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Daniel Lackner
PROVIDER: E-MTAB-2086 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Senescent is an irreversible form of cell cycle arrest initiated by damaged cell constituents and subsequent pro-oncogenic signaling. Replicative senescence in vitro can be considered a model for human aging. When fibroblasts are cultured under atmospheric oxygen conditions of 20%, typical of normal tissue culture procedure, fibroblasts generally reach their replicative capacity at 50-60 population doublings (PDs). When fibroblasts are cultured under normal physiological oxygen conditions of 3%, PDs increase about 30% relative to atmospheric levels. Hence while oxygen is a requirement for normal aerobic respiration, it can contribute to the total amount of oxidative stress to which cells are exposed to, leading to a long-term adverse effect in vitro. Inasmuch, cultures maintained under hyperoxic and hypoxic conditions provide a convenient model system for assessing the relationship between oxygen/oxidative stress and senescence. We used microarrays to profile the changes in global gene expression during aging and senescence of Imr90 cells under growth oxygen conditions of 3% and 20%. Imr90 cells at various population doubling timepoints (young, old, and senescent) grown separately under 3 and 20% oxygen growth conditions were selected for RNA extraction and hybridization on Affymetrix microarrays. Timepoints from cells grown under 3% and 20% oxygen conditions were age matched via population doublings to ensure accurate cross sample comparison.
2010-03-06 | E-GEOD-19018 | biostudies-arrayexpress
Project description:We stably infected IMR90 fibroblasts with lentiviral vectors expressing doxycycline-inducible TRF2dBdM or vector control. Cells were treated with 1mg/ml of doxycycline for 7 days to induce senescence in the cells expressing TRF2dBdM before collecting RNA. IMR90 cells, either young (passage 10, population doubling ~20) or old (passage 24, population doubling ~40-48) were also used as a model of replicative senescence. The transcriptomes were analyzed using RNA microarrays.
2021-02-12 | GSE153922 | GEO
Project description:Transcription profiling from young and pre-senescent IMR90 cells, transfected either with hTERT (pBabe-puro-hTERT) or vector control (pBabe-puro). Population doubling values are contained in Characteristics[generation] column.
2014-06-17 | E-MTAB-2087 | biostudies-arrayexpress
Project description:Noncoding RNAs include small transcripts, such as microRNAs and piwi-interacting RNAs, and a wide range of long noncoding RNAs (lncRNAs). Although many lncRNAs have been identified, only a small number of lncRNAs have been characterized functionally. Here, we sought to identify lncRNAs differentially expressed during replicative senescence. We compared lncRNAs expressed in proliferating, early-passage, 'young' human diploid WI-38 fibroblasts [population doubling (PDL) 20] with those expressed in senescent, late-passage, 'old' fibroblasts (PDL 52) by RNA sequencing (RNA-Seq). Numerous transcripts in all lncRNA groups (antisense lncRNAs, pseudogene-encoded lncRNAs, previously described lncRNAs and novel lncRNAs) were validated using reverse transcription (RT) and real-time, quantitative (q)PCR. Among the novel senescence-associated lncRNAs (SAL-RNAs) showing lower abundance in senescent cells, SAL-RNA1 (XLOC_023166) was found to delay senescence, because reducing SAL-RNA1 levels enhanced the appearance of phenotypic traits of senescence, including an enlarged morphology, positive β-galactosidase activity, and heightened p53 levels. Our results reveal that the expression of known and novel lncRNAs changes with senescence and suggests that SAL-RNAs play direct regulatory roles in this important cellular process. RNA was extracted from both young and senescent WI-38 cells and used for total RNA-Seq.
2016-02-08 | E-GEOD-77675 | biostudies-arrayexpress
Project description:Noncoding RNAs include small transcripts, such as microRNAs and piwi-interacting RNAs, and a wide range of long noncoding RNAs (lncRNAs). Although many lncRNAs have been identified, only a small number of lncRNAs have been characterized functionally. Here, we sought to identify lncRNAs differentially expressed during replicative senescence. We compared lncRNAs expressed in proliferating, early-passage, 'young' human diploid WI-38 fibroblasts [population doubling (PDL) 20] with those expressed in senescent, late-passage, 'old' fibroblasts (PDL 52) by RNA sequencing (RNA-Seq). Numerous transcripts in all lncRNA groups (antisense lncRNAs, pseudogene-encoded lncRNAs, previously described lncRNAs and novel lncRNAs) were validated using reverse transcription (RT) and real-time, quantitative (q)PCR. Among the novel senescence-associated lncRNAs (SAL-RNAs) showing lower abundance in senescent cells, SAL-RNA1 (XLOC_023166) was found to delay senescence, because reducing SAL-RNA1 levels enhanced the appearance of phenotypic traits of senescence, including an enlarged morphology, positive β-galactosidase activity, and heightened p53 levels. Our results reveal that the expression of known and novel lncRNAs changes with senescence and suggests that SAL-RNAs play direct regulatory roles in this important cellular process.
2016-02-08 | GSE77675 | GEO
Project description:Senescent is an irreversible form of cell cycle arrest initiated by damaged cell constituents and subsequent pro-oncogenic signaling. Replicative senescence in vitro can be considered a model for human aging. When fibroblasts are cultured under atmospheric oxygen conditions of 20%, typical of normal tissue culture procedure, fibroblasts generally reach their replicative capacity at 50-60 population doublings (PDs). When fibroblasts are cultured under normal physiological oxygen conditions of 3%, PDs increase about 30% relative to atmospheric levels. Hence while oxygen is a requirement for normal aerobic respiration, it can contribute to the total amount of oxidative stress to which cells are exposed to, leading to a long-term adverse effect in vitro. Inasmuch, cultures maintained under hyperoxic and hypoxic conditions provide a convenient model system for assessing the relationship between oxygen/oxidative stress and senescence. We used microarrays to profile the changes in global gene expression during aging and senescence of Imr90 cells under growth oxygen conditions of 3% and 20%.
2010-03-01 | GSE19018 | GEO
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:IMR90 cells were passaged until replicative senescence and compared with proliferating cells. We used RNA-Seq to detail the global programme of gene expression in human IMR90 replicative induced senescence
2014-11-26 | E-GEOD-53356 | biostudies-arrayexpress
Project description:Mammalian SIRT1 is a central regulator of metabolism and aging. This project is to analyze global phosphorylation levels of mammalian SIRT1 in proliferating and senescence states using human lung fibroblast IMR90, in order to explore the post-translational regulation of SIRT1 protein upon cellular senescence and its potential roles in the regulatory mechanisms of SIRT1 homeostasis.
2020-09-29 | PXD020081 | Pride
Project description:This SuperSeries is composed of the following subset Series: GSE3730: Replicative senescence in human fibroblasts GSE3731: Replicative senescence in post-selection HMECs Abstract: Replicative senescence is the state of irreversible proliferative arrest that occurs as a concomitant of progressive telomere shortening. By using cDNA microarrays and the gabriel system of computer programs to apply domain-specific and procedural knowledge for data analysis, we investigated global changes in gene transcription occurring during replicative senescence in human fibroblasts and mammary epithelial cells (HMECs). Here we report the identification of transcriptional "fingerprints" unique to senescence, the finding that gene expression perturbations during senescence differ greatly in fibroblasts and HMECs, and the discovery that despite the disparate nature of the chromosomal loci affected by senescence in fibroblasts and HMECs, the up-regulated loci in both types of cells show physical clustering. This clustering, which contrasts with the random distribution of genes down-regulated during senescence or up-regulated during reversible proliferative arrest (i.e., quiescence), supports the view that replicative senescence is associated with alteration of chromatin structure. Refer to individual Series
2006-03-06 | E-GEOD-4352 | biostudies-arrayexpress