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. Author manuscript; available in PMC: 2016 Jul 17.
Published in final edited form as: Circ Res. 2015 May 22;117(3):266–278. doi: 10.1161/CIRCRESAHA.117.305624

Figure 4. Inhibition of miR-33 increases mitochondrial respiration and ATP production that contributes to macrophage cholesterol efflux potential.

Figure 4

(A) Human macrophages were transfected with control anti-miR or anti-miR33 and the oxygen consumption rate was determined using the Seahorse XF24 Extracellular Flux Analyzer. Data depicted demonstrates mean ± SEM of n = 4 experiments. (B) Peritoneal macrophages were transfected with control miR, miR-33 mimics, control anti-miR or anti-miR33 for 48 h prior to the addition of apoA1 for 6h. Intracellular ATP levels were measured and are shown as either μM [ATP] per μg protein. (C) THP-1 macrophages transfected with control anti-miR or anti-miR33 for 24h were incubated with 1μCi/mL 3[H]-cholesterol and 37.5μg/mL acLDL for 24h prior to the addition of 25μg/mL apoA1 for 6h in the presence or absence of 10μM oligomycin. Percentage cholesterol efflux was determined relative to control and data shows mean ± SD of 6 replicates, and is representative of at least 3 independent experiments. (D) Peritoneal macrophages from either wild-type (WT) or Pgc-1α-/- mice were transfected with cont anti-miR or anti-miR33 and intracellular ATP was measured as in (B) above. Data shown are % change relative to control ± SD from 3 replicates, and is representative from at least 3 independent experiments. (E) Peritoneal or BMDM macrophages from either WT, Pgc-1α-/-, Pdk4-/- or Slc25a25-/- mice were transfected with anti-miRs and cholesterol efflux was measured as in (B). Data is shown as % increase in efflux to apoA1 by anti-miR33 compared to control anti-miR of 6 replicates, and is representative of n=3 independent experiments.