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ABSTRACT: p53 promotes revival stem cells in the regenerating intestine after severe radiation injury

PROVIDER: PRJNA910548 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22589000.fastq.gz	Fastqsanger.gz
	SRR22589001.fastq.gz	Fastqsanger.gz
	SRR22589002.fastq.gz	Fastqsanger.gz
	SRR22589003.fastq.gz	Fastqsanger.gz
	SRR22589004.fastq.gz	Fastqsanger.gz

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Single-Cell Transcriptomes of the Regenerating Intestine Reveal a Revival Stem Cell [part 1]

Project description:The weekly turnover of the intestinal epithelium is driven by multipotent, Lgr5+, crypt base columnar cells (CBCs). In response to injury, however, Lgr5+ cells are lost but then re-emerge and are required for successful recovery. How these resurgent Lgr5+ stem cells arise is unclear. We transcriptionally profiled single cells from regenerating intestinal epithelia and identified a unique cell type we term the revival stem cell (rSC). rSCs are mutually exclusive to CBCs and are distinguished by elevated expression of cell survival and DNA repair genes. In homeostasis, rSCs are extremely rare, but nevertheless give rise to all the major cell types of the intestine including crypt-villus axes. After damage rSCs display a 20-fold, Yap-dependent, transient expansion, reconstitute the Lgr5+ CBC compartment and are required to regenerate a functional intestine. These studies define a unique stem cell phenotype that is mobilized by damage to reconstitute the intestinal epithelium.

2019-02-28 | GSE117783 | GEO

Single-Cell Transcriptomes of the Regenerating Intestine Reveal a Revival Stem Cell [part 2]

2019-02-28 | GSE123515 | GEO

Single-Cell Transcriptomes of the Regenerating Intestine Reveal a Revival Stem Cell

Project description:Single-Cell Transcriptomes of the Regenerating Intestine Reveal a Revival Stem Cell

| PRJNA508975 | ENA

Single-Cell Transcriptomes of the Regenerating Intestine Reveal a Revival Stem Cell [part 1]

Project description:Single-Cell Transcriptomes of the Regenerating Intestine Reveal a Revival Stem Cell [part 1]

| PRJNA483187 | ENA

Single-Cell Transcriptomes of the Regenerating Intestine Reveal a Revival Stem Cell [part 2]

Project description:Single-Cell Transcriptomes of the Regenerating Intestine Reveal a Revival Stem Cell [part 2]

| PRJNA508976 | ENA

p53 suppresses MHC class II antigen presentation by the intestinal epithelium to protect intestinal stem cells upon radiation

Project description:To investigate the role of p53 in radiation-induced gastrointestinal syndrome, we performed gene expression profiling analysis using data obtained from RNA-seq of small intestine tissues from WT and p53-/- mice at 1 day post 12Gy total-body irradiation.

2023-11-10 | GSE226421 | GEO

Partial in vivo reprogramming enables injury-free intestinal regeneration via autonomous Ptgs1 induction [RNAseq_Fetal]

Project description:Tissue regeneration after injury involves the dedifferentiation of somatic cells, a natural adaptive reprogramming that leads to the emergence of injury-responsive cells with fetal-like characteristics. However, there is no direct evidence that adaptive reprogramming involves a shared molecular mechanism with direct cellular reprogramming. Here, we induced dedifferentiation of intestinal epithelial cells using OSKM (Oct4, Sox2, Klf4, and c-Myc) in vivo. The OSKM-induced forced dedifferentiation showed similar molecular features of intestinal regeneration, including a transition from homeostatic cell types to injury-responsive-like cell types. These injury-responsive-like cells, sharing gene signatures of revival stem cells and atrophy-induced villus epithelial cells, actively assisted tissue regeneration following damage. In contrast to normal intestinal regeneration involving Ptgs2 induction, the OSKM promotes autonomous production of prostaglandin E2 via epithelial Ptgs1 expression. These results indicate prostaglandin synthesis is a common mechanism for intestinal regeneration, but involves a different enzyme when partial reprogramming is applied to the intestinal epithelium.

2023-11-26 | GSE238056 | GEO

Partial in vivo reprogramming enables injury-free intestinal regeneration via autonomous Ptgs1 induction [RNAseq_IR]

2023-11-26 | GSE238055 | GEO

Extracts from sweet sorghum (Sorghum bicolor), a feedstock for biorefining, suppressed proliferation and elevated apoptosis in human colon cancer stem cells via suppression of Wnt/beta-catenin signaling pathway

Project description:In colorectal cancer, p53 is commonly inactivated, associated with chemo-resistance, and marks the transition from non-invasive to invasive disease. Cancers, including colorectal cancer, are thought to be diseases of aberrant stem cell populations, as stem cells are able to self-renew, making them long-lived enough to acquire mutations necessary to manifest the disease. We have shown that extracts from sweet sorghum stalk components eliminate colon cancer stem cells (CCSC) in a partial p53-dependent fashion. However, the underlying mechanisms are unknown. In the present study, CCSC were transfected with short hairpin-RNA against p53 (CCSC p53 shRNA) and treated with sweet sorghum phenolics extracted from different plant components (dermal layer, leaf, seed head and whole plant). While all components demonstrated anti-proliferative and pro-apoptotic effects in CCSC, phenolics extracted from the dermal layer and seed head were more potent in eliminating CCSC by elevating caspases 3/7 activity, PARP cleavage, and DNA fragmentation in a p53-dependent and p53-independent fashion, respectively. Further investigations revealed that the anti-proliferative and pro-apoptotic effects were associated with decreases in beta-catenin protein levels, and beta-catenin targets cyclin D1, cMyc, and survivin. These results suggest that the anti-proliferative and pro-apoptotic effects of sweet sorghum extracts against human colon cancer stem cells are via suppression of Wnt/beta-catenin pro-survival signaling in a p53-dependent (dermal layer) and partial p53-independent (seed head) fashion. LCMS used to identify phenolic compounds associated with extract activity

2014-05-01 | MTBLS69 | MetaboLights

Stroma provides an intestinal stem cell niche in the absence of epithelial Wnts

Project description:Wnt/b-catenin signaling supports intestinal homeostasis by regulating proliferation in the crypt. Multiple Wnts are expressed in Paneth as well as other intestinal epithelial and stromal cells. Ex vivo, Wnts secreted by Paneth cells can support intestinal stem cells when Wnt signaling is enhanced with supplemental R-Spondin 1 (RSPO1). However, in vivo, the source of Wnts in the stem cell niche is less clear. Genetic ablation of Porcn, an endoplasmic reticulum resident O-acyltransferase that is essential for the secretion and activity of all vertebrate Wnts, confirmed the role of intestinal epithelial Wnts in ex vivo culture. Unexpectedly, mice lacking epithelial Wnt activity (PorcnDel/Villin-Cre mice) had normal intestinal proliferation and differentiation, as well as successful regeneration after radiation injury, indicating epithelial Wnts are dispensable for these processes. Consistent with a key role for stroma in the crypt niche, intestinal stromal cells endogenously expressing Wnts and Rspo3 support the growth of PorcnDel organoids ex vivo without RSPO1 supplementation. Conversely, increasing pharmacologic PORCN inhibition, affecting both stroma and epithelium, reduced Lgr5 intestinal stem cells, inhibited recovery from radiation injury, and at the highest dose fully blocked intestinal proliferation. We conclude that epithelial Wnts are dispensable, and that stromal production of Wnts can fully support normal murine intestinal homeostasis. Microarray was performed on samples enriched for stromal or epithelial cells from small intestine from Porcn(Del)/Villin-Cre and Porcn(WT)/Villin-Cre male C57Bl/6 mice.

2014-04-19 | E-GEOD-56911 | biostudies-arrayexpress

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