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FTO suppresses cardiac fibrosis after myocardial infarction via m6A-mediated epigenetic modification [MeRIP-seq]

ABSTRACT: FTO suppresses cardiac fibrosis after myocardial infarction via m6A-mediated epigenetic modification [MeRIP-seq]

PROVIDER: PRJNA1080645 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28108178_1.fastq.gz	Fastqsanger.gz
	SRR28108178_2.fastq.gz	Fastqsanger.gz
	SRR28108179_1.fastq.gz	Fastqsanger.gz
	SRR28108179_2.fastq.gz	Fastqsanger.gz
	SRR28108180_1.fastq.gz	Fastqsanger.gz

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FTO suppresses cardiac fibrosis after myocardial infarction via m6A-mediated epigenetic modification [MeRIP-seq]

Project description:Cardiac fibrosis is common in cardiovascular diseases. N6-methyladenosine (m6A) is one of the most common modifications in eukaryotic mRNAs. Previous research has suggested that m6A modification is vital in cardiovascular diseases. The underlying targets of FTO were selected through transcriptome sequencing (RNA-seq) combined with methylated RNA immunoprecipitation sequencing (MeRIP-seq). According to MeRIP-seq and RNA-seq, FTO inhibited collagen synthesis in CFs.

2024-03-03 | GSE259328 | GEO

FTO suppresses cardiac fibrosis after myocardial infarction via m6A-mediated epigenetic modification

2024-03-01 | GSE257546 | GEO

FTO suppresses cardiac fibrosis after myocardial infarction via m6A-mediated epigenetic modification

Project description:FTO suppresses cardiac fibrosis after myocardial infarction via m6A-mediated epigenetic modification

| PRJNA1080202 | ENA

myocardial infarction in Reg3beta knock-out mice

Project description:Affymetrix microarray analysis of molecular changes after myocardial infarction. Samples of heart tissue were analyzed after myocardial infarction from WT and reg3beta knock-out mice. Samples from scar tissue and samples adjacent to the scar were analyzed. In the experiment we primarily compared infarction zone of wild-type to infarction zone of knock-out animals, and remote zone of wild-type to remote zone of knock-outs.

2015-06-29 | E-MTAB-2561 | biostudies-arrayexpress

Sequencing results of FTO overexpressing in papillary thyroid cells [meRIP-seq]

Project description:We tried to analyze the effect of FTO on papillary thyroid carcinoma. We constructed a FTO overexpression stable cell line of papillary thyroid carcinoma cells. We performed meRIP-seq sequencing analysis of the FTO overexpression stable transfer cell line to try to assess which genes were changed at the m6A level in papillary thyroid cancer cells by overexpressing FTO.

2022-05-06 | GSE199205 | GEO

The Obesity-associated Fto gene regulates activity of the dopaminergic midbrain circuitry [FTO KO]

Project description:Here we use MeRIP-Seq to analyze global adenosine methylation (m6A) in mRNAs in the midbrain and striatum of Fto-deficient mice. We find that Fto deficiency leads to increased methylation within a subset of mRNAs important for neuronal signaling, including many within the dopaminergic signaling pathway. Collectively, our results show that Fto regulates demethylation of specific mRNAs in vivo, and this activity relates to control of dopaminergic transmission. Profiling of m6A in midbrain and striatum from FTO knockout mice

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Licochalcone B alleviates Crohn’s Disease injury by targeting FTO [meRIP-seq]

Project description:To investigate the mechanism of demethylase FTO in Crohn's disease，We used m6A MeRIP-seq data from three normal colon samples and three TNBS-induced IBD colon samples of C57 mice for gene expression profiling.

2024-11-09 | GSE280813 | GEO

Effect of FTO-KD on m6A modification in GH3 cell line [MeRIP-seq]

Project description:Growth hormone-secreting pituitary adenomas account for approximately 10% of endocrine pituitary tumors and are pathologically classified into densely granulated adenomas (DGGH) and sparsely granulated adenomas (SGGH). m6A has been reported to play an important role in tumorigenesis and development, but its potential role in the pathogenesis of these two subtypes has not yet been thoroughly investigated. Consequently, we performed MeRIP-seq analysis of pituitary adenomas and the GH3 cell line. We observed that the expression of FTO was significantly increased in SGGH, leading to a reduction in m6A modification and a disruption of desmosome organization.

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Project description:Despite a substantial progress in diagnosis and therapy, acute myocardial infarction (MI) is a major cause of mortality in the general population. A novel insight into the pathophysiology of myocardial infarction obtained by studying gene expression should help to discover novel biomarkers of MI and to suggest novel strategies of therapy. The aim of our study was to establish gene expression patterns in leukocytes from acute myocardial infarction patients. ST-segment elevation myocardial infarction alters expression of several groups of genes. On admission, several genes and pathways that could be directly or indirectly linked with lipid/glucose metabolism, platelet function and atherosclerotic plaque stability were affected (signaling of PPAR, IL-10, IL-6). Analysis at discharge highlighted specific immune response (upregulation of immunoglobulins). Highly significant and substantial upregulation of SOCS3 and FAM20 genes expression in the first 4-6 days of myocardial infarction in all patients is the most robust observation of our work Twenty-eight patients with ST-segment elevation myocardial infarction (STEMI) were included. The blood was collected on the 1st day of myocardial infarction, after 4-6 days, and after 6 months. Control group comprised 14 patients with stable coronary artery disease (CAD), without history of myocardial infarction. Gene expression analysis was performed with Affymetrix GeneChipM-BM-. Human Gene 1.0 ST microarrays and GCS3000 TG system.

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