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Modulation of tRNA pool and tRNA fragments in obesity and diabetes; focus on their role in macrophage activation and exosome-mediated crosstalk with pancreatic beta cells

Project description

Transfer RNAs: a trigger for diabetes?

Chronic inflammation in obese individuals perturbs organ homeostasis and may lead to insulin resistance and type 2 diabetes (T2D). Emerging evidence indicates that macrophages play a major role in the metabolic switch that takes place prior to T2D development. The key objective of the EU-funded MATREX project is to further investigate the mechanisms responsible for macrophage activation. Researchers will focus on transfer RNAs (tRNA) known for their key role in protein translation. The rationale behind MATREX is that changes in the tRNA pool and integrity in adipose tissue and pancreatic islets may reflect metabolic changes in obesity that trigger T2D onset.

Objective

Obesity is a major public health concern and represents the strongest risk factor for type 2 diabetes (T2D) development. In T2D pathogenesis, inflammation contributes to multi-organ insulin resistance and pancreatic β-cell failure. Macrophages (Mφs) in adipose tissue and pancreatic islets play an important role in organ homeostasis, however their metabolic switch leads to chronic inflammation in obese individuals. The functional profile of obese Mφs reflects a high complexity, not explained by the classical model of pro-inflammatory activation. This suggests that unknown molecular modulators, higly sensitive to environmental changes, might control the activation of Mφs. Here I propose to investigate the role of transfer RNAs (tRNA) and tRNA fragmentation in in Mφ activation and diabetes pathogenesis. The ensemble of tRNAs in the cell is under strict regulation of nutrient availability and directly controls protein translation; also, tRNA fragmentation is controlled by stress factors and leads to the formation of tRNA fragments (tRFs), highly functional non-coding RNAs. I propose to study changes in tRNA pool and tRF signature in Mφs from adipose tissue and pancreatic islet using the db/db mouse model. I will analyse how protein translation is associated with tRNA pool, using ribosome profiling and computational methodologies. In addition, I will investigate the function of tRFs in the crosstalk between Mφs and β-cells via exosomes and their role in modulating β-cell function. I will use a Mφ-specific mouse model allowing the labeling of small RNAs in Mφs and the detection of the transferred molecules in β-cells. I will therefore combine high-throughput and in vivo innovative approaches to achieve the following aims: 1) Analyze the modulation of tRNA pool and translational in obese macrophages; 2) Investigating tRNA fragmentation and tRFs function in Mφs and β-cells during diabetes pathogenesis; 3) Study tRFs role in exosome-mediated Mφ to β-cell signaling.

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MSCA-IF - Marie Skłodowska-Curie Individual Fellowships (IF)

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Call for proposal

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(opens in new window) H2020-MSCA-IF-2020

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Coordinator

UNIVERSITE DE LAUSANNE
Net EU contribution

Net EU financial contribution. The sum of money that the participant receives, deducted by the EU contribution to its linked third party. It considers the distribution of the EU financial contribution between direct beneficiaries of the project and other types of participants, like third-party participants.

€ 191 149,44
Address
QUARTIER UNIL CENTRE - BATIMENT UNICENTRE
1015 LAUSANNE
Switzerland

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Region
Schweiz/Suisse/Svizzera Région lémanique Vaud
Activity type
Higher or Secondary Education Establishments
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Total cost

The total costs incurred by this organisation to participate in the project, including direct and indirect costs. This amount is a subset of the overall project budget.

€ 191 149,44
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