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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

Descrizione del progetto

Gli RNA transfer: fattori scatenanti del diabete?

L’infiammazione cronica in individui obesi altera l’omeostasi degli organi e può condurre all’insulino-resistenza e al diabete di tipo 2. Sempre più prove indicano che i macrofagi svolgono un ruolo di prim’ordine nella transizione metabolica che si verifica prima dello sviluppo del diabete di tipo 2. L’obiettivo chiave del progetto MATREX, finanziato dall’UE, consiste nell’indagare ulteriormente i meccanismi responsabili dell’attivazione macrofagica. I ricercatori si concentreranno sugli RNA transfer (tRNA), noti per il ruolo chiave svolto nella traduzione delle proteine. La logica alla base del progetto MATREX è la possibilità che le variazioni nei pool e nell’integrità di tRNA nel tessuto adiposo e nelle isole pancreatiche riflettano i cambiamenti metabolici nell’obesità che innescano l’insorgenza del diabete di tipo 2.

Obiettivo

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.

Campo scientifico (EuroSciVoc)

CORDIS classifica i progetti con EuroSciVoc, una tassonomia multilingue dei campi scientifici, attraverso un processo semi-automatico basato su tecniche NLP.

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Coordinatore

UNIVERSITE DE LAUSANNE
Contribution nette de l'UE
€ 191 149,44
Indirizzo
QUARTIER UNIL CENTRE - BATIMENT UNICENTRE
1015 LAUSANNE
Svizzera

Mostra sulla mappa

Regione
Schweiz/Suisse/Svizzera Région lémanique Vaud
Tipo di attività
Higher or Secondary Education Establishments
Collegamenti
Costo totale
€ 191 149,44