Abstract
Apart from the first family member, uncoupling protein 1 (UCP1), the functions of other UCPs (UCP2-UCP5) are still unknown. In analyzing our own results and those previously published by others, we have assumed that UCP's cellular expression pattern coincides with a specific cell metabolism and changes if the latter is altered. To verify this hypothesis, we analyzed the expression of UCP1-5 in mouse embryonic stem cells before and after their differentiation to neurons. We have shown that only UCP2 is present in undifferentiated stem cells and it disappears simultaneously with the initiation of neuronal differentiation. In contrast, UCP4 is simultaneously up-regulated together with typical neuronal marker proteins TUJ-1 and NeuN during mESC differentiation in vitro as well as during murine brain development in vivo. Notably, several tested cell lines express UCP2, but not UCP4. In line with this finding, neuroblastoma cells that display metabolic features of tumor cells express UCP2, but not UCP4. UCP2's occurrence in cancer, immunological and stem cells indicates that UCP2 is present in cells with highly proliferative potential, which have a glycolytic type of metabolism as a common feature, whereas UCP4 is strongly associated with non-proliferative highly differentiated neuronal cells.
Highlights
The subfamily of uncoupling proteins (UCP1-UCP5) belongs to the superfamily of mitochondrial carriers that are alleged to shuttle metabolic substrates across the mitochondrial inner membrane [1]
Using Western Blot analysis we have demonstrated that only UCP4 and not UCP2 is reliably present in mice neurons [16,17]
UCP2 is expressed in mouse embryonic stem cells
Summary
The subfamily of uncoupling proteins (UCP1-UCP5) belongs to the superfamily of mitochondrial carriers that are alleged to shuttle metabolic substrates across the mitochondrial inner membrane [1]. In contrast to other members of the family, UCPs were shown to mediate a proton leak across the membrane, which was demonstrated for all UCPs via different experimental systems ([2,3,4,5,6,7,8]). In the case of UCP1, proton transport in the presence of longchain fatty acids (FA) was linked to non-shivering thermogenesis [9,10]. The exact function(s) for UCP2-UCP5 remains elusive several interesting hypotheses exist. The most widespread one is that UCPs regulate reactive oxygen species (ROS) production in mitochondria. The fact that different UCPs (for example ‘‘brain’’-associated UCP2, UCP4 and UCP5) with the same putative proton transport function are present in the same tissue has until now remained insufficiently explained or confirmed
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
