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Human induced pluripotent cells treated with short-term Met deprival

ABSTRACT: Human induced pluripotent cells treated with short-term Met deprival

PROVIDER: PRJNA814054 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18272121.fastq.gz	Fastqsanger.gz
	SRR18272122.fastq.gz	Fastqsanger.gz
	SRR18272123.fastq.gz	Fastqsanger.gz
	SRR18272124.fastq.gz	Fastqsanger.gz
	SRR18272125.fastq.gz	Fastqsanger.gz

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RNA-seq of human induced pluripotent cells treated with short-term Met deprival

Project description:Human iPSCs require high amounts of methionine (Met). Met deprivation results in a rapid decrease in intracellular S-adenosyl-methionine (SAM), poising human iPSCs for differentiation and leading to apoptosis of undifferentiated cells. Met deprivation triggers a rapid metabolite change, including SAM, followed by reversible epigenetic modification. We show here that short-term Met deprivation impairs pluripotency network through epigenetic modification. The trimethylation of lysine 4 on histone H3 (H3K4me3) was dramatically affected compared to other histone modifications. Transcription start site (TSS) region of key pluripotent genes such as NANOG and OCT3/4 are specifically impacted upon short-term Met deprivation. Gene expression levels of these genes decreased, correlating to the loss of H3K4me3 marks. Upon differentiation, Met deprivation triggers a loss of the H3K27me3 in many mesendodermal genes, thereby switching from a bivalent to monovalent (H3K4me3) state. We concluded that Met metabolism maintains the pluripotent network with histone marks, and their loss potentiates differentiation.

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ChIP-seq of human induced pluripotent cells treated with short-term Met deprival

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ChIP-seq of human induced pluripotent cells treated with short-term Met deprival

Project description:ChIP-seq of human induced pluripotent cells treated with short-term Met deprival

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RNA-seq of human induced pluripotent cells treated with short-term Met deprival

Project description:RNA-seq of human induced pluripotent cells treated with short-term Met deprival

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Human induced pluripotent cells treated with short-term Met deprival

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

2022-12-05 | GSE198172 | GEO

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Cardioprotective signature of short-term caloric restriction

Project description:OBJECTIVE: To understand the molecular pathways underlying the cardiac preconditioning effect of short-term caloric restriction (CR). BACKGROUND: Lifelong CR has been suggested to reduce the incidence of cardiovascular disease through a variety of mechanisms. However, prolonged adherence to a CR life-style is difficult. Here we show how short-term CR protects the mouse heart from ischemia. METHODS: Male 10-12 wk old C57bl/6 mice were randomly assigned to an ad libitum (AL) diet with free access to regular chow, or CR, receiving 30% less food over a period of 7 days (d), prior to myocardial infarction (MI) via permanent coronary ligation. Prior to MI (d8), the left ventricles (LV) of AL and CR mice were collected for Western blot, DNA and microRNA (miR) analyses. In separate groups, infarct size, cardiac hemodynamics and protein abundance of caspase 3 was measured at d2 post-MI. RESULTS: This short-term model of CR was associated with cardio-protection, as evidenced by decreased infarct size (18.5±2.4% vs. 26.6±1.7%, N=10/group; P=0.01). cDNA and miR profiles pre-MI (N=5/group) identified genes modulated by short-term CR to be associated with circadian clock, oxidative stress, immune function, apoptosis, metabolism, angiogenesis, cytoskeleton and extracellular matrix (ECM). Western blots pre-MI revealed CR-associated increases in phosphorylated Akt and GSK3ß, reduced levels of phosphorylated AMPK and mitochondrial related proteins PGC-1α, cytochrome C and cyclooxygenase (COX) IV, with no differences in the levels of phosphorylated eNOS or MAPK (ERK1/2; p38). CONCLUSIONS: Short-term CR for only 7d represents a preconditioning strategy that limits infarct size. It is associated with a unique gene and miR signature, including the activation of specific pro-survival kinases. These findings may have implications for therapeutic use of short-term CR. .

2015-05-08 | GSE68646 | GEO

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