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Activation of imprinted gene Pw1 promotes cardiac fibrosis after ischemic injury [sham_and_MI]

ABSTRACT: Activation of imprinted gene Pw1 promotes cardiac fibrosis after ischemic injury [sham_and_MI]

PROVIDER: PRJNA971501 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29208200.fastq.gz	Fastqsanger.gz
	SRR29208201.fastq.gz	Fastqsanger.gz
	SRR29208202.fastq.gz	Fastqsanger.gz
	SRR29208203.fastq.gz	Fastqsanger.gz
	SRR29208204.fastq.gz	Fastqsanger.gz

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Similar Datasets

Activation of imprinted gene Pw1 promotes cardiac fibrosis after ischemic injury [sham_and_MI]

Project description:The activation of fibroblasts and production of extracellular matrix (ECM) after cardiac injury has been the focus of research on cardiac fibrosis. Whether imprinted genes play a role in the fibrogenesis or extracellular matrix production after heart damage has not been studied. Here, we show that the imprinted gene Pw1 directed ECM production by regulating de novo purine synthesis (DNPB) after myocardial infarction (MI). After MI, the DNA methylation of the imprinting control region (ICR) of Pw1 gene in the injured area was reduced and both alleles of Pw1 in fibroblasts are activated. Further, loss of Pw1 in fibroblasts can enhance cardiac function, reduce cardiac fibrosis and extracellular matrix secretion after cardiac injury. To screen the targets of PW1, we contrasted chromatin immunoprecipitation (ChIP)-seq and RNA-seq using the injured left ventricles at 7 days post-MI, we next found PW1 binds directly upstream of the Pfas gene that encodes one of the DNPB enzymes phosphoribosylformylglycinamidine synthase (PFAS) in heart after injury. Similarly, specific knockout of pfas in fibroblasts also improves cardiac function and reduces ECM production. Moreover, de novo purine biosynthesis is necessary for ECM production in activated fibroblasts. These observations implicate understanding the mechanism of Pw1 in the repair of cardiac injury will provide new ideas for the treatment of cardiovascular diseases.

2024-12-04 | GSE232259 | GEO

Activation of imprinted gene Pw1 promotes cardiac fibrosis after ischemic injury [control_and_Pw1 CKO]

2024-12-04 | GSE232326 | GEO

Activation of imprinted gene Pw1 promotes cardiac fibrosis after ischemic injury [ChIP-seq]

2024-12-04 | GSE279698 | GEO

Activation of imprinted gene Pw1 promotes cardiac fibrosis after ischemic injury [control_and_Pfas CKO RNA-seq]

2024-12-04 | GSE231979 | GEO

Activation of imprinted gene Pw1 promotes cardiac fibrosis after ischemic injury

Project description:Activation of imprinted gene Pw1 promotes cardiac fibrosis after ischemic injury

| PRJNA971616 | ENA

Activation of imprinted gene Pw1 promotes cardiac fibrosis after ischemic injury [ChIP-seq]

Project description:Activation of imprinted gene Pw1 promotes cardiac fibrosis after ischemic injury [ChIP-seq]

| PRJNA1174112 | ENA

Activation of imprinted gene Pw1 promotes cardiac fibrosis after ischemic injury [control_and_Pw1 CKO]

Project description:Activation of imprinted gene Pw1 promotes cardiac fibrosis after ischemic injury [control_and_Pw1 CKO]

| PRJNA971619 | ENA

Activation of imprinted gene Pw1 promotes cardiac fibrosis after ischemic injury [control_and_Pfas CKO RNA-seq]

Project description:Activation of imprinted gene Pw1 promotes cardiac fibrosis after ischemic injury [control_and_Pfas CKO RNA-seq]

| PRJNA970349 | ENA

Activation of imprinted gene Pw1 promotes cardiac fibrosis after ischemic injury

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

2024-12-04 | GSE232327 | GEO

PW1/Peg3 expression regulates the key properties that determine mesoangioblast stem cell competence

Project description:Mesoangioblasts are vessel-associated progenitor cells that show therapeutic promise for the treatment of muscular dystrophy. Mesoangioblasts have the ability to undergo skeletal muscle differentiation and cross the blood vessel wall regardless of the developmental stage at which they are isolated. Here we show that PW1/Peg3 is expressed at high levels in mesoangioblasts obtained from mouse, dog and human tissues and its level of expression correlates with their myogenic competence. Silencing PW1/Peg3 markedly inhibits myogenic potential of mesoangioblasts in vitro through MyoD degradation. Moreover, lack of PW1/Peg3 abrogates mesoangioblast ability to cross the vessel wall and to engraft into damaged myofibers through the modulation of the junctional adhesion molecule-A. We conclude that PW1/Peg3 function is essential for conferring proper mesoangioblast competence and that the determination of PW1/Peg3 levels in human mesoangioblasts may serve as a biomarker to identify the best donor populations for therapeutic application in muscular dystrophies. Ctrl Mesoangioblasts (MABs) transduced with a Lentiviral vector shControl (2 replicates, Ctrl_1 and Ctrl_2) and shPW1 Mesoangioblasts transduced with a Lentiviral vector shPW1 (2 replicates, PW1-siRna_1 and PW1-siRna_2)

2015-01-19 | E-GEOD-64334 | biostudies-arrayexpress

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