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Transcriptome analysis of Endothelin-3 or Neurotensin treated MuSCs

ABSTRACT: Transcriptome analysis of Endothelin-3 or Neurotensin treated MuSCs

PROVIDER: PRJNA982099 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24887626.fastq.gz	Fastqsanger.gz
	SRR24887627.fastq.gz	Fastqsanger.gz
	SRR24887628.fastq.gz	Fastqsanger.gz
	SRR24887629.fastq.gz	Fastqsanger.gz
	SRR24887630.fastq.gz	Fastqsanger.gz

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Transcriptome analysis of Endothelin-3 or Neurotensin treated MuSCs

Project description:GPCRs have emerged as crucial regulators of muscle stem cell (MuSC) quiescence, yet the specific repertoire of GPCRs in quiescent MuSCs and the underlying regulatory network remain largely elusive. By employing pharmacological and inducible-genetic methods, we have identified two niche-derived GPCR ligands, endothelin-3 (ET-3) and neurotensin (NT), which bind to EDNRB and NTSR2 receptors, respectively, reinforcing the maintenance of MuSC quiescence. To comprehensively unravel the molecular mechanisms underlying the inhibitory effects of ET-3 and NT on MuSC activation, we conducted RNA sequencing (RNA-seq) analysis on FACS-purified MuSCs that underwent a 5-day in vitro treatment with ET-3 or NT

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Unravelling the mechanism of neurotensin recognition by neurotensin receptor 1

Project description:The conformational ensembles of G-protein coupled receptors (GPCRs) include inactive and active states. Spectroscopy techniques, including NMR, show that agonists, antagonists and other ligands shift the ensemble toward specific states depending on the pharmacological efficacy of the ligand. How receptors recognize ligands and the kinetic mechanism underlying this population shift is poorly understood. Here, we investigate the kinetic mechanism of neurotensin recognition by neurotensin receptor 1 (NTS1) using 19F-NMR, hydrogen-deuterium exchange mass spectrometry and stopped-flow fluorescence spectroscopy. Our results indicate slow-exchanging conformational heterogeneity on the extracellular surface of ligand-bound NTS1. Numerical analysis of the kinetic data of neurotensin binding to NTS1 shows that ligand recognition follows an induced fit mechanism, in which conformational changes occur after neurotensin binding. This approach is applicable to other GPCRs to provide insight into the kinetic regulation of ligand recognition by GPCRs.

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Project description:Neurotensin(NTS), a gut hormone, is known to impact whole body energy metabolism. Here we investigated the impact of neurotensin on the liver in fed (ad libitum) and fasted (22h) female mice livers from NTS wild type (WT) and knockout (KO) mice. Our goal was to investigate the regulation of energy metabolism pathways in the liver that are regulated by neurotensin, specifically lipid uptake and mitochondrial metabolism.

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Project description:Skeletal muscle possesses the ability to adapt its size in response to milieus, which is called plasticity. Overload like resistance training induces the increment of muscle mass called muscle hypertrophy. Muscle stem cells (also known as muscle stem cells) function to supply new nuclei for myofiber during the overload in muscle. Using compensatory hypertrophy in plantaris muscles, we isolated MuSCs from plantaris muscles 4 days after surgery. Control MuSCs were also prepared from sham plantaris muscles.

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Project description:Calorie-rich foods, particularly those high in fat and sugar, evoke pleasure in both humans and animals. However, prolonged consumption of such foods may reduce their hedonic value, potentially contributing to obesity. Here, we investigated this phenomenon in mice on a chronic high-fat diet (HFD). While these mice preferred high-fat food over regular chow in their home cages, they showed reduced interest in calorie-rich foods in a no-effort setting. This paradoxical decrease in hedonic feeding has been reported previously, but its neurobiological basis remains unclear. We found that in regular diet mice, neurons in the lateral nucleus accumbens projecting to the ventral tegmental area (NAcLat→VTA) encoded hedonic feeding behaviors. In HFD mice, this behavior was reduced and uncoupled from neural activity. Optogenetic stimulation of the NAcLat→VTA pathway increased hedonic feeding in regular diet mice but not in HFD mice, though this behavior was restored when HFD mice returned to a regular diet. HFD mice exhibited reduced neurotensin expression and release in the NAcLat→VTA pathway. Furthermore, neurotensin knockout in the NAcLat and neurotensin receptor blockade in the VTA each abolished optogenetic-induced hedonic feeding behavior. Enhancing neurotensin signaling via overexpression normalized aspects of diet-induced obesity, including weight gain and hedonic feeding. Altogether, our findings identify a neural circuit mechanism linking the devaluation of hedonic foods with obesity.

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