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. 2016 Jun 16;100(5):1113–1124. doi: 10.1189/jlb.3A1015-463R

Figure 8. mTOR inhibition modulates macrophage mitochondrial metabolism.

Figure 8.

(A and B) OCR was assessed via Seahorse Bioscience flux analyzer in macrophages stimulated as indicated for 16 h in presence of vehicle (veh; A) or torin (B) at baseline and after injection of flurorcarbonyl cynade phenylhydrazon (max), or rotenone/antimycin (rot/ant). (C) pMACS were stimulated as indicated in the presence of veh or torin for 16 h, and glycolytic rate was estimated by ECAR using a Seahorse Bioscience metabolic flux analyzer. (D) pMACs were stimulated with PBS or LPS, and mitochondrial OCR (total OCR − nonmitochondrial OCR) was measured at baseline and after injection of indicated metabolic inhibitors [UK5099 (pyruvate); etomoxir (eto; FA oxidation); BPTES (glutamine)]. (E) Macrophages were treated with palm-LPS in the presence of veh or the indicated metabolic inhibitors, and cell death was assessed by LDH release. rapa, rapamycin. Bar graphs report means ± se for a minimum of 3 experiments, each performed in triplicate. *P < 0.05 for BSA-PBS vs. palm-LPS or veh vs. inhibitor; #P < 0.05 for veh vs. torin.