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PPARg T166 phosphorylation-mediated lipid synthesis sustains the reparative function of macrophages during tissue repair [CUT&RUN]

ABSTRACT: PPARg T166 phosphorylation-mediated lipid synthesis sustains the reparative function of macrophages during tissue repair [CUT&RUN]

PROVIDER: PRJNA1123759 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29402146_1.fastq.gz	Fastqsanger.gz
	SRR29402146_2.fastq.gz	Fastqsanger.gz

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PPARg T166 phosphorylation-mediated lipid synthesis sustains the reparative function of macrophages during tissue repair [ChIP-seq]

Project description:Macrophages exhibit a reparative phenotype that supports tissue repair and remodeling in response to tissue injury. However, the metabolic requirements that support this process have remained incompletely understood. Here, we showed that posttranslational modification (PTM) of peroxisome proliferator-activated receptor g (PPARg) regulated lipid synthesis in response to wound microenvironmental cues and that metabolic rewiring orchestrated the function of reparative macrophages. In injured tissues, repair signaling attenuated macrophage PPARg threonine 166 (T166) phosphorylation, which induced a partially active PPARg program with increased binding activity to the regulator regions of lipid synthesis-associated genes, thereby activating lipogenesis. The accumulated lipids served as signaling molecules, triggering signal transducer and activator of transcription 3 (STAT3)-mediated growth factor expression, and supporting the synthesis of phospholipids for the expansion of the endoplasmic reticulum (ER), which is required for the secretion of proteins. Genetic or pharmacological inhibition of PPARg T166 phosphorylation promoted the reparative function of macrophages and facilitated tissue regeneration. In summary, we identified that PPARg T166-regulated lipid biosynthesis was essential for the anabolic demands of the activation and function of macrophages and provided a rationale for therapeutic targeting of tissue repair.

2024-07-30 | GSE252900 | GEO

PPARg T166 phosphorylation-mediated lipid synthesis sustains the reparative function of macrophages during tissue repair [RNA-seq]

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PPARg T166 phosphorylation-mediated lipid synthesis sustains the reparative function of macrophages during tissue repair [CUT&RUN]

2024-07-30 | GSE269832 | GEO

PPARg T166 phosphorylation-mediated lipid synthesis sustains the reparative function of macrophages during tissue repair

Project description:PPARg T166 phosphorylation-mediated lipid synthesis sustains the reparative function of macrophages during tissue repair

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PPARg T166 phosphorylation-mediated lipid synthesis sustains the reparative function of macrophages during tissue repair [RNA-seq]

Project description:PPARg T166 phosphorylation-mediated lipid synthesis sustains the reparative function of macrophages during tissue repair [RNA-seq]

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PPARg T166 phosphorylation-mediated lipid synthesis sustains the reparative function of macrophages during tissue repair [ChIP-seq]

Project description:PPARg T166 phosphorylation-mediated lipid synthesis sustains the reparative function of macrophages during tissue repair [ChIP-seq]

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Blockage of PPARg T166 phosphorylation enhances the inducibility of beige adipocytes and improves metabolic dysfunctions

Project description:Beige adipocytes in mammalian white adipose tissue (WAT) can reinforce fat catabolism and energy expenditure. Promoting beige adipocyte biogenesis is a tantalizing tactic for combating obesity and its associated metabolic disorders. Here, we report that a previously unidentified phosphorylation pattern (Thr166) in the DNA-binding domain of PPARg regulates the inducibility of beige adipocytes. This unique posttranslational modification (PTM) pattern influences allosteric communication between PPARg and DNA or coactivators, which impedes the PPARg-mediated transactivation of beige cell-related gene expression in WAT. The genetic mutation mimicking T166 phosphorylation (p-T166) hinders the inducibility of beige adipocytes. In contrast, genetic or chemical intervention in this PTM pattern favors beige cell formation. Moreover, inhibition of p-T166 attenuates metabolic dysfunction in obese mice. Our results uncover a mechanism involved in beige cell fate determination. Moreover, our discoveries provide a promising strategy for guiding the development of novel PPARg agonists for the treatment of obesity and related metabolic disorders.

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PPARg T166 phosphorylation-mediated lipid synthesis sustains the reparative function of macrophages during tissue repair

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

2024-07-30 | GSE269834 | GEO

Project description:RNAseq of PPARg T166 mutated adipocytes

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Non-canonical glutamine transamination sustains efferocytosis by coupling redox buffering to oxidative phosphorylation

Project description:Non-canonical glutamine transamination sustains efferocytosis by coupling redox buffering to oxidative phosphorylation

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