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Fatty Acid Oxidation and Glycolysis Regulate Skin ECM Homeostasis by Shifting Fibroblasts between Catabolism and Anabolism (BeadChip)

ABSTRACT: Transcriptome profiling of human radiation-induced skin fibrosis and normal age matched control revealed a shift from catabolic to anabolic pathways in fibrosis. The paper has been published: https://www.nature.com/articles/s42255-018-0008-5?WT.feed_name=subjects_metabolism

ORGANISM(S): Homo sapiens

PROVIDER: GSE98159 | GEO | 2018/12/27

REPOSITORIES: GEO

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Fatty Acid Oxidation and Glycolysis Regulate Skin ECM Homeostasis by Shifting Fibroblasts between Catabolism and Anabolism

Project description:This SuperSeries is composed of the SubSeries listed below. The paper has been published: https://www.nature.com/articles/s42255-018-0008-5?WT.feed_name=subjects_metabolism

2018-12-27 | GSE98160 | GEO

Fatty Acid Oxidation and Glycolysis Regulate Skin ECM Homeostasis by Shifting Fibroblasts between Catabolism and Anabolism (RNA-Seq)

Project description:Transcriptome profiling of murine skin fibrosis, and its treatment through CD36highCD90+ fibroblast transplantation revealed the most significant alterations to be involved in fatty acid metabolism and glycolysis. The paper has been published: https://www.nature.com/articles/s42255-018-0008-5?WT.feed_name=subjects_metabolism

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Digital RNA with pertUrbation of Genes (DRUG-Seq) of LN-229 glioblastoma cells treated with 20 different drugs at two time points

Project description:DRUG-Seq is a miniatruized and multiplexed RNA-Seq protocol described in Ye et al., 2018 (https://www.nature.com/articles/s41467-018-06500-x) To determine transcriptional changes upon drug perturbation in LN-229 glioblastoma cells, we profiled 20 drug responses across two time-points (6 and 22 hours) by DRUG-Seq

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Applying plexDIA analysis to newly synthesized proteome samples generated using a semi-automated enrichment protocol

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2023-10-19 | PXD043817 | Pride

Fatty Acid Oxidation and Glycolysis Regulate Skin ECM Homeostasis by Shifting Fibroblasts between Catabolism and Anabolism

Project description:Fatty Acid Oxidation and Glycolysis Regulate Skin ECM Homeostasis by Shifting Fibroblasts between Catabolism and Anabolism

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Coupled catabolism and anabolism in autocatalytic RNA sets.

Project description:The ability to process molecules available in the environment into useable building blocks characterizes catabolism in contemporary cells and was probably critical for the initiation of life. Here we show that a catabolic process in collectively autocatalytic sets of RNAs allows diversified substrates to be assimilated. We modify fragments of the Azoarcus group I intron and find that the system is able to restore the original native fragments by a multi-step reaction pathway. This allows in turn the formation of catalysts by an anabolic process, eventually leading to the accumulation of ribozymes. These results demonstrate that rudimentary self-reproducing RNA systems based on recombination possess an inherent capacity to assimilate an expanded repertoire of chemical resources and suggest that coupled catabolism and anabolism could have arisen at a very early stage in primordial living systems.

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Epigenetic Regulation of Chondrocyte Catabolism and Anabolism in Osteoarthritis.

Project description:Osteoarthritis (OA) is one of the most prevalent forms of joint disorder, associated with a tremendous socioeconomic burden worldwide. Various non-genetic and lifestyle-related factors such as aging and obesity have been recognized as major risk factors for OA, underscoring the potential role for epigenetic regulation in the pathogenesis of the disease. OA-associated epigenetic aberrations have been noted at the level of DNA methylation and histone modification in chondrocytes. These epigenetic regulations are implicated in driving an imbalance between the expression of catabolic and anabolic factors, leading eventually to osteoarthritic cartilage destruction. Cellular senescence and metabolic abnormalities driven by OA-associated risk factors appear to accompany epigenetic drifts in chondrocytes. Notably, molecular events associated with metabolic disorders influence epigenetic regulation in chondrocytes, supporting the notion that OA is a metabolic disease. Here, we review accumulating evidence supporting a role for epigenetics in the regulation of cartilage homeostasis and OA pathogenesis.

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Increased glutamine catabolism mediates bone anabolism in response to WNT signaling.

Project description:WNT signaling stimulates bone formation by increasing both the number of osteoblasts and their protein-synthesis activity. It is not clear how WNT augments the capacity of osteoblast progenitors to meet the increased energetic and synthetic needs associated with mature osteoblasts. Here, in cultured osteoblast progenitors, we determined that WNT stimulates glutamine catabolism through the tricarboxylic acid (TCA) cycle and consequently lowers intracellular glutamine levels. The WNT-induced reduction of glutamine concentration triggered a general control nonderepressible 2-mediated (GCN2-mediated) integrated stress response (ISR) that stimulated expression of genes responsible for amino acid supply, transfer RNA (tRNA) aminoacylation, and protein folding. WNT-induced glutamine catabolism and ISR were ?-catenin independent, but required mammalian target of rapamycin complex 1 (mTORC1) activation. In a hyperactive WNT signaling mouse model of human osteosclerosis, inhibition of glutamine catabolism or Gcn2 deletion suppressed excessive bone formation. Together, our data indicate that glutamine is both an energy source and a protein-translation rheostat that is responsive to WNT and suggest that manipulation of the glutamine/GCN2 signaling axis may provide a valuable approach for normalizing deranged protein anabolism associated with human diseases.

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Project description:The malignant energetic demands are satisfied through glycolysis, glutaminolysis and de novo synthesis of fatty acids, while the host curses with a state of catabolism and systemic inflammation. The concurrent inhibition of both, tumor anabolism and host catabolism, and their effect upon tumor growth and whole animal metabolism, have not been evaluated. We aimed to evaluate in colon cancer cells a combination of six agents directed to block the tumor anabolism (orlistat + lonidamine + DON) and the host catabolism (growth hormone + insulin + indomethacin). Treatment reduced cellular viability, clonogenic capacity and cell cycle progression. These effects were associated with decreased glycolysis and oxidative phosphorylation, leading to a quiescent energetic phenotype, and with an aberrant transcriptomic landscape showing dysregulation in multiple metabolic pathways. The in vivo evaluation revealed a significant tumor volume inhibition, without damage to normal tissues. The six-drug combination preserved lean tissue and decreased fat loss, while the energy expenditure got decreased. Finally, a reduction in gene expression associated with thermogenesis was observed. Our findings demonstrate that the simultaneous use of this six-drug combination has anticancer effects by inducing a quiescent energetic phenotype of cultured cancer cells. Besides, the treatment is well-tolerated in mice and reduces whole animal energetic expenditure and fat loss.

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Targeting HDAC6 to treat heart failure with preserved ejection fraction, Mouse heart LC-MS with PTMscan

Project description:Heart failure with preserved ejection fraction (HFpEF) poses therapeutic challenges due to the limited treatment options. Building upon our previous research that demonstrates the efficacy of histone deacetylase 6 (HDAC6) inhibition in a genetic cardiomyopathy model, we investigate HDAC6’s role in HFpEF due to their shared mechanisms of inflammation and metabolism. Here, we show that inhibiting HDAC6 with TYA-018 effectively reverses established heart failure and its associated symptoms in HFpEF mouse models. Additionally, in mice lacking the Hdac6 gene, HFpEF progression is delayed and they are resistant to TYA-018’s effects. The efficacy of TYA-018 is comparable to a sodium-glucose cotransporter 2 (SGLT2) inhibitor, and their combination shows enhanced effects. Mechanistically, TYA-018 restores gene expression related to hypertrophy, fibrosis, and mitochondrial energy production in HFpEF heart tissues. Furthermore, TYA-018 also inhibits activation of human cardiac fibroblasts and enhances mitochondrial respiratory capacity in cardiomyocytes. In this work, our findings show that HDAC6 impacts heart pathophysiology and is a promising target for HFpEF treatment.

2024-01-17 | PXD048363 | Pride

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