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

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

PROVIDER: PRJNA894863 | ENA |

REPOSITORIES: ENA

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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]

| PRJNA892116 | ENA

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

| PRJNA894864 | ENA

MiR-29ab regulates intestinal stem cell fate through fatty-acid-oxidation-related energy metabolism [after 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 3 day after irradiation.

2023-12-31 | GSE216669 | GEO

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

2023-12-31 | GSE216122 | GEO

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.

2024-10-30 | GSE272659 | GEO

Repair of airway epithelia requires metabolic rewiring towards fatty acid oxidation

Project description:Repair of airway epithelia requires metabolic rewiring towards fatty acid oxidation

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Reduced fatty acid synthesis and enhanced oxidation promote human definitive endoderm differentiation

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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Induction of lipid oxidation gene expression by polyunsaturated fatty acids of marine origin in small intestine of mice

Project description:Dietary polyunsaturated fatty acids (PUFA) act as potent natural hypolipidemics and are linked to many health benefits in humans and in animal models. Mice fed long-term a high fat diet, in which medium-chain alpha linoleic acid (ALA) was partially replaced by long-chain docosahexaenoic (DHA) and eicosapentaenoic (EPA) fatty acids, showed reduced accumulation of body fat and prevention of insulin resistance, besides increased mitochondrial beta-oxidation in white adipose tissue and decreased plasma lipids. ALA, EPA and DHA all belong to PUFA of n-3 series. The intestine is a gatekeeper organ for ingested lipids. To examine the potential contribution of the intestine in the beneficial effects of EPA and DHA, this study assessed gene expression changes using whole genome microarray analysis on small intestinal scrapings. The main biological process affected was lipid metabolism. Fatty acid uptake, peroxisomal and mitochondrial beta-oxidation, and omega-oxidation of fatty acids were all increased. Quantitative real time PCR and intestinal fatty acid oxidation measurements ([14C(U)]-palmitate) confirmed significant gene expression differences in a dose-dependent manner. Furthermore, no major changes in the expression of lipid metabolism genes were observed in colonic scrapings. In conclusion, we show that marine n-3 fatty acids regulate small intestinal gene expression patterns. Since this organ contributes significantly to whole organism energy use, this adaptation of the small intestine may contribute to the complex and observed beneficial physiological effects of these natural compounds under conditions that will normally lead to development of obesity and diabetes.

2009-04-01 | GSE11936 | GEO

Yap regulates fatty acid oxidation in skeletal muscle

Project description:Yap regulates fatty acid oxidation in skeletal muscle

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Quiescent endothelial cells upregulate fatty acid β-oxidation for vasculoprotection via redox homeostasis

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

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