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

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

PROVIDER: PRJNA894864 | 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:MiR-29ab regulates intestinal stem cell fate through fatty-acid-oxidation-related energy metabolism [before irradiation]

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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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Effect of inhibition of fatty acid beta-oxidation on gene expression of double-negative T cells

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DNA damage-activated mitochondrial fatty acid oxidation drives senescence

Project description:Cellular senescence is a stress-induced irreversible cell cycle arrest involved in tumor suppression and aging. Many stresses, such as telomere shortening and oncogene activation, induce senescence by damaging nuclear DNA. However, the mechanisms linking DNA damage to senescence remain unclear. Here, we show that DNA damage response (DDR) signaling to mitochondria triggers senescence. A genome-wide siRNA screen implicated the outer mitochondrial transmembrane protein BNIP3 in senescence induction. We found that BNIP3 is a substrate of the DDR kinase ATM and contributes to an increase in the number of mitochondrial cristae upon DNA damage. Stable isotope labeling metabolomics indicated that this increase in cristae enhances the oxidation of fatty acids to acetyl-CoA. Notably, pharmacological activation of fatty acid oxidation alone induced senescence both in vitro and in vivo. Our findings suggest that mitochondrial energy metabolism plays a critical role in senescence induction and is a potential intervention target to control 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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Long-chain fatty acid β-oxidation regulates embryonic development by H3K18 acetylation in mice [RNA-seq]

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

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

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