Abstract:
:Etomoxir (ETO) is a widely used small-molecule inhibitor of fatty acid oxidation (FAO) through its irreversible inhibitory effects on the carnitine palmitoyl-transferase 1a (CPT1a). We used this compound to evaluate the role of fatty acid oxidation in rapidly proliferating T cells following costimulation through the CD28 receptor. We show that ETO has a moderate effect on T cell proliferation with no observable effect on memory differentiation, but a marked effect on oxidative metabolism. We show that this oxidative metabolism is primarily dependent upon glutamine rather than FAO. Using an shRNA approach to reduce CPT1a in T cells, we further demonstrate that the inhibition of oxidative metabolism in T cells by ETO is independent of its effects on FAO at concentrations exceeding 5 μM. Concentrations of ETO above 5 μM induce acute production of ROS with associated evidence of severe oxidative stress in proliferating T cells. In aggregate, these data indicate that ETO lacks specificity for CTP1a above 5 μM, and caution should be used when employing this compound for studies in cells due to its non-specific effects on oxidative metabolism and cellular redox.
journal_name
Sci Repjournal_title
Scientific reportsauthors
O'Connor RS,Guo L,Ghassemi S,Snyder NW,Worth AJ,Weng L,Kam Y,Philipson B,Trefely S,Nunez-Cruz S,Blair IA,June CH,Milone MCdoi
10.1038/s41598-018-24676-6subject
Has Abstractpub_date
2018-04-19 00:00:00pages
6289issue
1issn
2045-2322pii
10.1038/s41598-018-24676-6journal_volume
8pub_type
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