Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

In vivo reprogramming drives dedifferentiation and enhances liver regeneration

ABSTRACT: In vivo reprogramming drives dedifferentiation and enhances liver regeneration

PROVIDER: PRJNA604183 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10994409_1.fastq.gz	Fastqsanger.gz
	SRR10994409_2.fastq.gz	Fastqsanger.gz
	SRR10994410_1.fastq.gz	Fastqsanger.gz
	SRR10994410_2.fastq.gz	Fastqsanger.gz
	SRR10994411_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 62

Similar Datasets

In vivo reprogramming drives dedifferentiation and enhances liver regeneration

Project description:Mammalian tissues have a limited regenerative capacity. Previous studies showed that dedifferentiation contributes to tissue regeneration in non-mammalian vertebrate species such as zebrafish and newt. However, dedifferentiation is rarely observed in mammalian tissues even in the neonatal stage and therefore artificial induction of dedifferentiation might enhance regeneration in mammalian tissues. Here we demonstrate that short-term expression of Yamanaka 4 factors (4F) induces dedifferentiation and proliferation in the liver by using lineage-traceable, hepatocyte-specific 4F inducible mouse model. Global transcriptome analysis shows that 4F expression transiently reduces the expression of hepatic-lineage markers and induces the expression of a large set of proliferative markers and epigenetic modifiers along with global epigenetic changes as assessed by DNA-accessibility analysis. More importantly, lineage-tracing experiments showed that 4F-expressing hepatocytes acquire liver stem/progenitor cell markers, suggesting that 4F induces partial reprogramming. Moreover, 4F enhances MyoD-mediated transdifferentiation in the liver, suggesting that 4F endows hepatocytes with plasticity. Lastly, 4F expression attenuated liver injury associated with more proliferative capacity and better survival rate, indicating that 4F enhances liver regeneration. Taken together, these results demonstrate that liver-specific 4F expression induces dedifferentiation and promotes liver regeneration.

2022-04-27 | GSE144600 | GEO

Cardiac-tbx20 overexpression enhances heart regeneration by promoting cardiomyocytes dedifferentiation and endocardial activation

Project description:Cardiac-tbx20 overexpression enhances heart regeneration by promoting cardiomyocytes dedifferentiation and endocardial activation

| PRJNA605096 | 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

Fibroblast Dedifferentiation as a Determinant of Successful Regeneration

Project description:Fibroblast Dedifferentiation as a Determinant of Successful Regeneration

| PRJNA698552 | ENA

The Right Ventricular Fibroblast Secretome Drives Cardiomyocyte Dedifferentiation

Project description:The Right Ventricular Fibroblast Secretome Drives Cardiomyocyte Dedifferentiation

| PRJNA552980 | ENA

Meteorin-like enhances aged muscle regeneration

Project description:Meteorin-like enhances aged muscle regeneration

| PRJNA896603 | ENA

Transient epigenetic reprogramming during adult zebrafish muscle regeneration

Project description:Genomic reprogramming and cellular dedifferentiation are critical to the success of de novo tissue regeneration in lower vertebrates such as zebrafish and axolotl. ChIP-seq of the histone modifications H3K27Ac, H3K27me3, and H3K4me3 was used to characterize early epigenetic changes in a zebrafish in vivo model of adult muscle regeneration.

2019-12-06 | GSE137304 | GEO

In vivo activation of a conserved microRNA program induces robust mammalian heart regeneration (array)

Project description:Heart failure is a leading cause of mortality and morbidity in the developed world, partly because mammals lack the ability to regenerate heart tissue. Whether this is due to evolutionary loss of regenerative mechanisms present in other organisms or to an inability to activate such mechanisms is currently unclear. Here, we decipher mechanisms underlying heart regeneration in adult zebrafish and show that the molecular regulators of this response are conserved in mammals. We identified miR-99/100 and Let-7a/c, and their protein targets smarca5 and fntb, as critical regulators of cardiomyocyte dedifferentiation and heart regeneration in zebrafish. Although human and murine adult cardiomyocytes fail to elicit an endogenous regenerative response following myocardial infarction, we show that in vivo manipulation of this molecular machinery in mice results in cardiomyocyte dedifferentiation and improved heart functionality after injury. These data provide a proof-of-concept for identifying and activating conserved molecular programs to regenerate the damaged heart. Analysis of miRNA levels in regenerating zebrafish hearts

2014-11-20 | E-GEOD-62386 | biostudies-arrayexpress

Vitamin B12 is a limiting factor for in vivo reprogramming

Project description:Reprogramming in vivo using OCT4, SOX2, KLF4 and MYC (OSKM) triggers cell dedifferentiation, which is considered of relevance for tissue repair and regeneration. However, little is known about the metabolic requirements of this process. We found that antibiotic depletion of the gut microbiota abolished in vivo reprogramming. Analysis of bacterial metagenomes from stool samples of wild type (WT) and OSKM mice treated with doxycycline led us to identify vitamin B12 as a key factor for in vivo reprogramming, which is partly supplied by the microbiome. We report that B12 demand increases during reprogramming due to enhanced expression of enzymes in the methionine cycle, and supplementing B12 levels both in vitro and in vivo enhances the efficiency of OSKM reprogramming.

2023-08-07 | GSE154149 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data