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ABSTRACT: Physical Exercise-induced Extracellular Vesicles Ameliorate Chronic Pancreatitis via Inhibiting STING-Interferon Signaling

PROVIDER: PRJNA1009945 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25782127_1.fastq.gz	Fastqsanger.gz
	SRR25782127_2.fastq.gz	Fastqsanger.gz
	SRR25782128_1.fastq.gz	Fastqsanger.gz
	SRR25782128_2.fastq.gz	Fastqsanger.gz
	SRR25782129_1.fastq.gz	Fastqsanger.gz

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Physical Exercise-induced Extracellular Vesicles Ameliorate Chronic Pancreatitis via Inhibiting STING-Interferon Signaling

Project description:Physical Exercise-induced Extracellular Vesicles Ameliorate Chronic Pancreatitis via Inhibiting STING-Interferon Signaling

2023-08-28 | GSE241626 | GEO

Physical Exercise-induced Extracellular Vesicles Ameliorate Chronic Pancreatitis via Inhibiting STING-Interferon Signaling

Project description:Physical Exercise-induced Extracellular Vesicles Ameliorate Chronic Pancreatitis via Inhibiting STING-Interferon Signaling

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E-MEXP-804

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Physical activity diminish fatigue and systemic interferon response in multiple sclerosis

Project description:Objective: To evaluate gene expression profiles in multiple sclerosis (MS) patients who improved their fatigue status after a program of physical exercise and to compare them with healthy controls (HC). Methods: A prospective longitudinal study was conducted. Gene expression in whole blood was profiled at baseline in 7 healthy controls and also in 7 fatigued-MS patients. Patients underwent a physical exercise program for 6 months, and their fatigue status and gene expression profiles were again analyzed at the end of this program. Results: MS patients showed a significant activation of genes participating in the systemic interferon response in comparison with healthy controls. Fatigue improved at the end of the physical activity program, and, in parallel, systemic activation of interferon related genes disappeared. Conclusions: Fatigue improvement following an exercise program is associated to down modulation of interferon activity at the systemic level in MS patients. Our results provide a biological basis for the observed benefit of physical exercise in MS.

2015-09-27 | E-MTAB-2973 | biostudies-arrayexpress

Exercise reverses dysregulation of T cell-related function in blood leukocytes of patients with PD

Project description:Parkinson’s disease (PD) is a common neurodegenerative disease with movement and balance impairments. It has been shown that physical exercise could ameliorate balance impairments and improve life quality of PD patients. However, the related mechanisms of benefit of exercise are still poorly understood, especially in the peripheral immune system. The present study aimed to utilize sensitive high-throughput transcriptome analyses to investigate potentially favorable effects of physical exercise in leukocytes.

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Project description:Transcription profiling of pancreas from Wistar or WBN/Kob rats to study chronic pancreatitis

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Blood flow-restricted resistance exercise (BFRE) alters the surface profile, miRNA cargo and functional impact of circulating extracellular vesicles

Project description:In this study, we provide evidence that ischemic exercise, conducted as blood flow-restricted resistance exercise, promote changes in the micro-RNA cargo of circulating extracellular vesicles in healthy volunteers.

2020-04-12 | GSE136997 | GEO

Regulatory T cells promote endurance exercise adaptation by shielding muscle mitochondria from damage

Project description:<p>Exercise enhances physical performance and reduces the risk of many disorders such as cardiovascular disease, type 2 diabetes, dementia and cancer. Exercise characteristically incites an inflammatory response, notably in skeletal muscles. While some effector mechanisms have been identified, regulatory elements activated in response to exercise remain obscure. Here, we have addressed the roles of Foxp3+CD4+ regulatory T cells (Tregs) in the healthful activities of exercise via immunologic, transcriptomic, histologic, metabolic and biochemical analyses of acute and chronic murine exercise models. Exercise rapidly induced expansion of the muscle Treg compartment, thereby guarding against over-exuberant production of interferon gamma and consequent metabolic disruptions, particularly mitochondrial aberrancies. Importantly, the performance-enhancing effects of exercise training were dampened in the absence of Tregs. Thus, exercise is a natural Treg booster with therapeutic potential in disease and aging contexts.</p>

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STING signalling is terminated through ESCRT-dependent microautophagy of vesicles originating from recycling endosomes

Project description:Stimulator of interferon genes (STING) is essential for the type I interferon response against a variety of DNA pathogens. Upon emergence of cytosolic DNA, STING translocates from the endoplasmic reticulum (ER) to the Golgi where STING activates the downstream kinase TBK1, then to lysosome through recycling endosomes (REs) for its degradation. Although the molecular machinery of STING activation is extensively studied and defined, the one underlying STING degradation and inactivation has not yet been fully elucidated. Here we show that STING is degraded by the endosomal sorting complexes required for transport (ESCRT)-driven microautophagy. Airyscan super-resolution microscopy and correlative light/electron microscopy suggest that STING-positive vesicles of an RE origin are directly encapsulated into Lamp1-positive compartments. Screening of mammalian Vps genes, the yeast homologues of which regulate Golgi-to-vacuole transport, shows that ESCRT proteins are essential for the STING encapsulation into Lamp1-positive compartments. Knockdown of Tsg101 and Vps4, components of ESCRT, results in the accumulation of STING vesicles in the cytosol, leading to the sustained type I interferon response. Knockdown of Tsg101 in human primary T cells leads to an increase the expression of interferon-stimulated genes. STING undergoes K63-linked ubiquitination at lysine 288 during its transit through the Golgi/REs, and this ubiquitination is required for STING degradation. Our results reveal a molecular mechanism that prevents hyperactivation of innate immune signalling, which operates at REs.

2023-01-24 | PXD039411 | Pride

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