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Mitochondrial function in metabolism and inflammation
Third-party funded project
Project title Mitochondrial function in metabolism and inflammation
Principal Investigator(s) Handschin, Christoph
Organisation / Research unit Departement Biomedizin / Pharmakologie (Handschin),
Departement Biozentrum / Growth & Development (Handschin)
Project start 01.12.2012
Probable end 30.11.2013
Status Completed
Abstract

Properly regulated mitochondrial function is crucial for maintaining cellular and organismal health. Accordingly, mutations in mitochondrial genes, dysregulated mitochondrial biogenesis or impaired mitochondrial function are associated with various diseases. For example, mitochondrial dysfunction has been implicated in the etiology of various metabolic pathologies, including obesity and type 2 diabetes. Our lab is interested in studying the regulation of mitochondrial biogenesis and oxidative metabolism, which is under the control of the peroxisome proliferator-activated receptor g coactivator 1 (PGC-1) protein family, in skeletal muscle, but also other tissues with a high energetic demand. In muscle, PGC-1a is a key regulator of adaptation to endurance exercise including a fiber-type switch towards oxidative type I and IIa muscle fibers and a boost in mitochondrial biogenesis and function. Inversely, absence of proper PGC-1a activity in muscle results in impaired exercise tolerance and fiber damage accompanied by tissue and systemic inflammation. Importantly, such a sterile, chronic inflammation is the hallmark of many metabolic diseases. Interestingly, very similar to oxidative tissues such as skeletal muscle, brown fat or liver, adequate regulation of mitochondrial function is a key event in the activation and specification of macrophages, T cells and other immune cells. Therefore, a profound understanding of mitochondrial function is crucial to advance our knowledge in regard to the physiological and pathophysiological adaptations that mediate the cross-talk between metabolism and inflammation. In our studies, we characterize mitochondrial number, morphology and function using a number of different approaches such as electron microscopy, gene expression and enzymatic assays. Unfortunately, we currently lack access to an instrument that directly determines mitochondrial respiration rates and substrate utilization in a format that allows the analysis of human and mouse samples in limiting quantities and under ambient oxygen concentrations that correspond to those that are physiologically observed in situ. The Seahorse XF96 Extracellular Flux Analyzer combined with a SCI-tive NN Workstation would enable several groups from the Biozentrum and the Department of Biomedicine to measure these key parameters of cellular function in a way that is accessible to non-specialists. Therefore, we hope for positive evaluation and approval of our R’Equip Grant application for the acquisition of such an instrument.

Financed by Swiss National Science Foundation (SNSF)
   

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