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. 2021 Jan 1;11(5):2424–2441. doi: 10.7150/thno.46873

Figure 2.

Figure 2

PPARγ interfered NLRP3 oligomerization and NLRP3-ASC interaction. (A) Immunoblot analysis of mature IL-1β in the supernatant and indicated components and PPARγ in the cell lysates of NLRP3 inflammasome-reconstituted HEK293T cells transfected with indicated components. (B) Immunoblot analysis of mature IL-1β in the supernatant, and pro-IL-1β and PPARγ in the cell lysates of NLRP3 inflammasome-reconstituted HEK293T cells transfected with indicated components. Rosiglitazone (Rosi, 20μM) was treated for 24 h after transfection. (C-D) Immunoblot analysis of ASC oligomerization in HEK293T cells transfected with ASC, NLRP3 and PPARγ. PPARγ band is labeled with arrowhead and a non-specific band is labeled with asterisk in (D). (E) Immunoprecipitation and immunoblot analysis of the interaction between Myc-tagged NLRP3 and HA-tagged NLRP3 in HEK293T cells. Quantification of Myc-tagged NLRP3 relative to the level of HA-tagged NLRP3 from four independent experiments. (F) Immunoprecipitation and immunoblot analysis of the interaction between HA-tagged NLRP3 and ASC in HEK293T cells. Quantification of ASC relative to the level of HA-tagged NLRP3 from three independent experiments. *P < 0.05 and ***P < 0.001 by one-way ANOVA with Fisher's LSD test in (E-F). Representative blots are from three independent experiments. Experiment replicates are shown in Figure S11.