Transcriptomic profiling of senescent human stromal cells upon medicinal intervention with rutin
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ABSTRACT:
PROVIDER: PRJNA786575 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17143620_1.fastq.gz | Fastqsanger.gz | |||
| SRR17143620_2.fastq.gz | Fastqsanger.gz | |||
| SRR17143621_1.fastq.gz | Fastqsanger.gz | |||
| SRR17143621_2.fastq.gz | Fastqsanger.gz | |||
| SRR17143622_1.fastq.gz | Fastqsanger.gz |
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Project description:Aging and age-related pathologies can be delayed by specifically targeting the senescence-associated secretory phenotype (SASP), a hallmark feature of senescent cells. Achieving the goal using natural or synthetic agents would have a tremendous impact on the quality of lifespan and burden of age-related chronic diseases. We report the potential of rutin, a bioactive phytochemical component derived from natural plants specifically ginkgo boliva, in targeting senescent cells via suppression of the SASP. This study demonstrates the efficacy of rutin as medicinal agent in controlling the influence of senescent human stromal cells and provides a strong rationale for its future use in aging intervention and geriatric medicine.
2023-11-02 | GSE190279 | GEO
Project description:Aging and age-relataed pathologies can be delayed by specifically targeting the senescence-associated secretory phenotype (SASP), a hallmark feature of senescent cells. Achieving the goal using small molecules would have a tremendous impact on the quality of lifespan and burden of age-related chronic diseases. We report the potential of curcumin, a polyphenol constituent (up to ∼5%) of the traditional medicine known as turmeric, in targeting senescent cells via induction of programmed cell death. This study demonstrates the impact of curcumin as a medicinal compound on the expression profile of senescent cells and provides a strong rationale for its future application in geriatric medicine.
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Project description:Aging and age-related pathologies can be delayed by specifically targeting the senescence-associated secretory phenotype (SASP), a hallmark feature of senescent cells. Achieving the goal using small molecule inhibitors would have a tremendous impact on the quality of lifespan and burden of age-related chronic diseases. We report the potential of alpha lipoic acid (ALA), a naturally existing antioxidant, in targeting senescent cells via induction of programmed cell death. This study demonstrates the impact of alpha-lipoic acid as a medicinal compound on the expression profile of senescent cells and provides a strong rationale for its future use in geriatric medicine.
2022-12-31 | GSE156184 | GEO
Project description:Aging and age-related pathologies can be delayed by specifically targeting the senescence-associated secretory phenotype (SASP), a hallmark feature of senescent cells. Achieving the goal using small molecule inhibitors would have a tremendous impact on the quality of lifespan and burden of age-related chronic diseases. We report the potential of grape seed extract (GSE), a naturally existing source of phytochemicals including terpenoids, carotenoids, and flavonoids, in targeting senescent cells via induction of programmed cell death. This study demonstrates the impact of GSE as a medicinal compound on the expression profile of senescent cells and provides a strong rationale for its future use in geriatric medicine.
2021-10-04 | GSE156301 | GEO
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.
2009-03-30 | GSE13330 | GEO
Project description:Aging and age-relataed pathologies can be delayed by specifically targeting the senescence-associated secretory phenotype (SASP), a hallmark feature of senescent cells. Achieving the goal using small molecules would have a tremendous impact on the quality of lifespan and burden of age-related chronic diseases. We report the potential of two metabolic molecules, NAD+ and NMN, to control the development of the pro-inflammatory phenotype of senescent human stromal cells. This study discloses the impact of NAD+ and NMN on the expression profile of senescent cells and provides a framework for future anti-aging administration with clear rationale.
2022-12-31 | GSE156038 | GEO
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
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. Experiment Overall Design: Human foreskin BJ fibroblasts were mock or Bleomycin sulfate-treated (100ug/ml, Sigma, St. Louis, MO) for 24 hrs. Replicatively senescent fibroblasts were obtained by continuous passage. After 72 hr serum-starvation, RNA was collected using TRIzol (Invitrogen, Carlsbad, CA). Biotinylated cRNA was hybridized to Affymetrix Human Genome U133 Plus 2.0 GeneChips (Affymetrix, Santa Clara, CA) by the Washington University Microarray Facility. Experiment Overall Design: There were 4, 6, and 6 samples for SIPS, RS, and young respectively: Experiment Overall Design: - Stress-induced premature senescence (GSM336347..GSM336379) Experiment Overall Design: - Replicative Senescent (GSM336385..GSM336573) Experiment Overall Design: - Young (GSM336574..GSM336628) Experiment Overall Design: Microarray quality control, analysis, and clustering (UPGMA by Centroid) were performed using dChip (May, 2008 release). All GeneChip comparisons had a cut-off basis of a lower bound of 90% confidence of fold-change â?¥1.5 and expression intensity difference â?¥75.
2009-04-04 | E-GEOD-13330 | biostudies-arrayexpress
Project description:Damage of the intestinal epithelial barrier by xenobiotics or reactive oxygen species and a dysregulated immune response are both factors involved in the pathogenesis of inflammatory bowel diseases (IBD). Curcumin and rutin are polyphenolic compounds known to have anti-oxidant and anti-inflammatory activities, but their mechanism(s) of action are yet to be fully elucidated. Mdr1a-/- mice spontaneously develop intestinal inflammation, predominantly in the colon, with pathology similar to IBD, so this mouse model is relevant for studying diet-gene interactions and potential effects of foods on remission or development of IBD. This study tested whether the addition of curcumin or rutin to the diet would alleviate colonic inflammation in mdr1a-/- mice. Using whole-genome microarrays, the effect of dietary curcumin on gene expression in colon tissue was also investigated. Twelve mice were randomly assigned to each of three diets; control (AIN-76A), control + 0.2% curcumin or control + 0.1% rutin and monitored from the age of 7 to 24 weeks. Curcumin, but not rutin, significantly reduced histological signs of colonic inflammation in mdr1a-/- mice. Microarray and pathway analyses suggested that the effect of dietary curcumin on colon inflammation could be via an up-regulation of xenobiotic metabolism and a down-regulation of pro-inflammatory pathways probably mediated by PXR and PPARï¡ activation of RXR. These results reveal the potential of global gene expression and pathway analyses to study and better understand the effect of foods in colonic inflammation. Experiment Overall Design: Twelve mice were randomly assigned to each of three diets; control (AIN-76A), control + 0â¢2% curcumin or control + 0â¢1% rutin and monitored from the age of 7 to 24 weeks. As only curcumin significantly reduced colonic HIS, comparison of the gene expression levels in colon was carried out using total RNA from colon tissue of four mdr1a-/- mice from the control group (high HIS) and four mdr1a-/- mice from the curcumin group (low HIS). A reference design with eight arrays was used for this comparison, where each individual RNA sample was hybridized in the array with the reference RNA, totalizing 4 biological replicates per treatment.
2008-06-11 | E-GEOD-10684 | biostudies-arrayexpress
Project description:Transcriptomic profiling of human senescent cells in the setting of curcumin intervention
| PRJNA658072 | ENA