Abstract
The mitochondrial uncoupling protein family includes at least five members (UCP1 - UCP5), which are implicated in the pathophysiology of different diseases such as obesity, diabetes type II, ischemia, cancer and neurodegenerative disorders. In contrast to the well-defined function of UCP1 in thermogenesis, the uncertain role and expression patterns of subfamily members are controversially discussed. Recently, we suggested that UCP2 and UCP4 expression is tightly connected to a certain type of cell metabolism (1,2). Surprisingly, highly homologous UCP1 and UCP3 with similar proton transport functions were reported to be present in BAT. To get a hint about the reason for this expression pattern, we aimed to quantify the amounts of UCP3 in mouse tissues under different conditions in this study and compare it to the UCP1 amounts in BAT. For this we designed a specific antibody against UCP3, which we have validated using UCP3 knockout mice tissue and recombinant mouse UCP3. We confirmed that UCP3 is expressed in brown adipose tissue, gastrocnemius muscle, scapular muscle and the heart. Using an established WB approach with recombinant UCPs, we were able to show for the first time, that the amount of the expressed UCP3 in BAT is much higher compared to the muscle samples, but still considerably lower than the amount of UCP1 in BAT determined previously (1). UCP3 abundance in muscles fluctuates strongly in different mice and between various muscle types of the same mouse already under physiological conditions. The results of this study support the hypothesis about different biological function of both, UCP1 and UCP3.1. Smorodchenko,A et al. Mol Cell Neurosci. 2011 Aug;47(4):244-53.2. Rupprecht,A. et al. PLoS One. 2012;7(8):e41406.
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