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. 2015 Nov 3;125(12):4592–4600. doi: 10.1172/JCI83260

Figure 5. SIRT3 levels modify NLRP3 activation and acetylation of SOD2.

Figure 5

(A) Representative immunoblot of steady-state levels of SIRT1, SIRT2, SIRT3, and SIRT5 following the siRNA knockdown of each isoform in THP-1 cells. The relative changes represent the values from 3 separate experiments. (B) IL-1β release in response to inflammasome activation in the sirtuin knockdown THP-1 cells (n = 11). (C) Inflammasome activation with wild-type and deacetylase mutant SIRT3 overexpression in THP-1 cells (n = 4). *P < 0.05. (D) Mitochondrial superoxide dismutase activity in PBMC mitochondria isolated in the fasted and fed states (n = 4). (E) Representative immunoblot analysis of relative SOD2 protein acetylation on K68 in the fed and fasted states. The relative quantitative change in SOD2 acetylation is shown in F (n = 4). (G) Histogram showing relative release of IL-1β in control and SIRT3-overexpressing cells in response to inflammasome activation in the absence of or presence of ROS inhibition with mitoTEMPO and DPI (n = 5). (H) Histogram showing the same studies as performed in F, with the exception of testing the effect of SIRT3 knockdown rather than overexpression (n = 5). Statistical analysis of changes in IL-1β secretion levels was performed using 2-way ANOVA and analysis of changes in SOD2 activity and acetylation was performed using a paired 2-tailed t test.