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MiR-29ab regulates intestinal stem cell fate through fatty-acid-oxidation-related energy metabolism [before irradiation]

ABSTRACT: MiR-29ab regulates intestinal stem cell fate through fatty-acid-oxidation-related energy metabolism [before irradiation]

PROVIDER: PRJNA892116 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21973580_1.fastq.gz	Fastqsanger.gz
	SRR21973580_2.fastq.gz	Fastqsanger.gz
	SRR21973581_1.fastq.gz	Fastqsanger.gz
	SRR21973581_2.fastq.gz	Fastqsanger.gz
	SRR21973582_1.fastq.gz	Fastqsanger.gz

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MiR-29ab regulates intestinal stem cell fate through fatty-acid-oxidation-related energy metabolism [before irradiation]

Project description:To investigate the mechanism of miR-29ab in regulation of intestinal stem cells and partipation in epithelium post-injury regeneration, we established miR-29ab1-/- mice and applied irradiation to damage stem cell. We then performed gene expression profiling analysis using data obtained from RNA-seq of intestinal crypts from WT and miR-29ab1-/- mice before and after irradiation.

2023-12-31 | GSE216122 | GEO

MiR-29ab regulates intestinal stem cell fate through fatty-acid-oxidation-related energy metabolism [after irradiation]

Project description:MiR-29ab regulates intestinal stem cell fate through fatty-acid-oxidation-related energy metabolism [after irradiation]

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MiR-29ab regulates intestinal stem cell fate through fatty-acid-oxidation-related energy metabolism

Project description:MiR-29ab regulates intestinal stem cell fate through fatty-acid-oxidation-related energy metabolism

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MiR-29ab regulates intestinal stem cell fate through fatty-acid-oxidation-related energy metabolism [after irradiation]

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DNA damage-activated mitochondrial fatty acid oxidation drives senescence

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Project description:Metabolic remodeling is one of the earliest events that occur during the early differentiation of embryonic stem cells (ESCs), but how these metabolic changes are regulated and participate in the cell differentiation is still largely undissected. Here, we define the fatty acid metabolism as a key player in definitive endoderm (DE) differentiation from human ESCs. During DE differentiation, lipogenesis is decreased while fatty acid β oxidation is enhanced. This dynamic is due to the phosphorylation of lipogenic enzyme acetyl-CoA carboxylase (ACC), which is mediated by AMP-activated protein kinase (AMPK) and inhibits the de novo fatty acid synthesis. More importantly, inhibition of fatty acid synthesis by either its inhibitors or AMPK agonist, significantly promotes the human endoderm differentiation, while blockade of the fatty acid oxidation by genetic manipulation or chemical antagonists impairs the differentiation. The de novo fatty acid synthesis inhibition and fatty acid β oxidation maintaining contribute to the accumulation of cellular acetyl-CoA, which is the essential substrate for protein acetylation. Further study reveals that SMAD3 acetylation and the subsequent subcellular localization exhibit significant change upon interfering fatty acid metabolism. Mechanistically, the accumulation of cellular acetyl-CoA guarantees the acetylation of key transcription factor SMAD3, which further causes the nuclear localization and activation of SMAD signaling pathway to promote DE differentiation. Thus, our current study reveals a fatty acid synthesis/oxidation shift during early differentiation and presents an instructive role of fatty acid metabolism in regulating human early endoderm differentiation.

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Project description:Little is known about metabolic changes accompanying endothelial cell (EC) quiescence. Nonetheless, when dysfunctional, quiescent ECs (QECs) contribute to multiple cardiovascular diseases. ECs need fatty acid β-oxidation (FAO) for proliferation. Surprisingly, we now report that QECs are not hypo-metabolic, but upregulate FAO >3-fold higher than proliferating ECs (PECs), not to support biomass or energy production, but to sustain the TCA cycle for redox homeostasis through NADPH production. Hence, inhibition of FAO-controlling CPT1A promotes EC dysfunction (anti-fibrinolysis, leukocyte infiltration, barrier disruption) by increasing oxidative stress in CPT1AΔEC mice with endothelial CPT1A loss. Mechanistically, Notch1 orchestrates the use of FAO for redox balance in QECs. Supplementation of acetate (metabolized to acetyl-CoA) induces vasculoprotection against oxidative stress and EC dysfunction in CPT1AΔEC mice, possibly creating therapeutic opportunities. Thus, ECs use FAO for vasculoprotection against their high oxygen (oxidative stress-prone) milieu, and for different metabolic purposes dependent on their proliferation versus quiescence status.

2018-09-12 | E-MTAB-6595 | biostudies-arrayexpress