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Partial in vivo reprogramming enables injury-free intestinal regeneration via autonomous Ptgs1 induction.

ABSTRACT: Partial in vivo reprogramming enables injury-free intestinal regeneration via autonomous Ptgs1 induction.

PROVIDER: PRJNA997871 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25396035.fastq.gz	Fastqsanger.gz
	SRR25396036.fastq.gz	Fastqsanger.gz
	SRR25396136.fastq.gz	Fastqsanger.gz
	SRR25396037.fastq.gz	Fastqsanger.gz
	SRR25396137.fastq.gz	Fastqsanger.gz

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

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

| PRJNA997892 | ENA

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

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

| PRJNA997893 | ENA

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

Partial in vivo reprogramming enables injury-free intestinal regeneration via autonomous Ptgs1 induction.

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-11-24 | GSE238057 | GEO

Characterization of hepatic gene expression during liver regeneration in response to partial hepatectomy

Project description:This SuperSeries is composed of the following subset Series: GSE20425: Hepatic gene expression during liver regeneration in response to partial hepatectomy: early time points (0.5h,1h,2h,4h) GSE20426: Hepatic gene expression during liver regeneration in response to partial hepatectomy: late time points (24h, 38h, 48h) Refer to individual Series

2011-02-16 | E-GEOD-20427 | biostudies-arrayexpress

Expression data from rat hepatocyte during liver regeneration after partial hepatectomy

Project description:The recovery of liver mass is mainly mediated by proliferation and enlargement of hepatocytes after partial hepatectomy. Studying the gene expression profiles of hepatocytes after partial hepatectomy will be helpful in exploring the mechanism of liver regeneration. We used microarrays to further highlight the regulatory role of hepatocyte in liver regeneration at gene transcription level. Rat liver regeneration after partial hepatectomy (PH) is a good model to study the regulation of cell proliferation. We isolated hepatocytes from regenerating liver at 9 time points (2, 6, 12,24, 30, 36, 72, 120, and 168h) after PH and measured gene expression profiles of hepatocytes from 2h to 168h with rat Genome 230 2.0 gene chip. Each sample corresponding to one time point was hybridized onto one array. The experiment was repeated 3 times for each time point. In total, 10 time points were measured and 0h was used control group. After careful quality control analyses of each chip, Affymetrix GCOS 2.0 software was used to analyze the data. The relevance of gene expression profiles and biological processes was analyzed by bioinformatics and systems biology.

2014-02-28 | E-GEOD-55434 | biostudies-arrayexpress

DNA dioxygenase Tet2 regulates liver regeneration after partial hepatectomy [dateset2]

Project description:To investigate how liver macrophages regulate liver regeneration after partial hepatectomy, we isolate the macrophages 0, 24, and 48h after partial hepatectomy(PHx). We performed gene expression profiling analysis using data obtained from RNA-seq of liver macrophages 0,24,48h after partial hepatectomy.

2025-05-21 | GSE233515 | GEO

Expression data from rat hepatocyte during liver regeneration after partial hepatectomy

2014-02-28 | GSE55434 | GEO

FOXF1 transcription factor promotes lung regeneration after partial pneumonectomy

Project description:FOXF1, a member of the forkhead box family of transcription factors, has been previously shown to be critical for lung development, homeostasis, and injury responses. However, the role of FOXF1 in lung regeneration is unknown. Herein, we performed partial pneumonectomy, a model of lung regeneration, in mice lacking one Foxf1 allele in endothelial cells (PDGFb-iCre/Foxf1fl/+ mice). Endothelial cell proliferation was significantly reduced in regenerating lungs from mice deficient for endothelial Foxf1. Decreased endothelial proliferation was associated with delayed lung regeneration as shown by reduced respiratory volume in Foxf1-deficient lungs. FACS-sorted endothelial cells isolated from regenerating PDGFb-iCre/Foxf1fl/+ and control lungs were used for RNAseq analysis to identify FOXF1 target genes. Foxf1 deficiency altered expression of numerous genes including those regulating extracellular matrix remodeling (Timp3, Adamts9) and cell cycle progression (Cdkn1a, Cdkn2b, Cenpj, Tubb4a), which are critical for lung regeneration. Deletion of Foxf1 increased Timp3 mRNA and protein, decreasing MMP14 activity in regenerating lungs. ChIPseq analysis for FOXF1 and histone methylation marks identified DNA regulatory regions with the Cd44, Cdkn1a, and Cdkn2b genes, indicating they are direct FOXF1 targets. Thus FOXF1 stimulates lung regeneration following partial pneumonectomy via direct transcriptional regulation of genes critical for extracellular matrix remodeling and cell cycle progression.

2017-09-12 | GSE100149 | GEO

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