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

ABSTRACT: 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

ORGANISM(S): Mus musculus

PROVIDER: GSE98157 | 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 (BeadChip)

Project description: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

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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

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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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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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PTH Promotes Bone Anabolism by Stimulating Aerobic Glycolysis via IGF Signaling.

Project description:Teriparatide, a recombinant peptide corresponding to amino acids 1-34 of human parathyroid hormone (PTH), has been an effective bone anabolic drug for over a decade. However, the mechanism whereby PTH stimulates bone formation remains incompletely understood. Here we report that in cultures of osteoblast-lineage cells, PTH stimulates glucose consumption and lactate production in the presence of oxygen, a hallmark of aerobic glycolysis, also known as Warburg effect. Experiments with radioactively labeled glucose demonstrate that PTH suppresses glucose entry into the tricarboxylic acid cycle (TCA cycle). Mechanistically, the increase in aerobic glycolysis is secondary to insulin-like growth factor (Igf) signaling induced by PTH, whereas the metabolic effect of Igf is dependent on activation of mammalian target of rapamycin complex 2 (mTORC2). Importantly, pharmacological perturbation of glycolysis suppresses the bone anabolic effect of intermittent PTH in the mouse. Thus, stimulation of aerobic glycolysis via Igf signaling contributes to bone anabolism in response to PTH.

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