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. Author manuscript; available in PMC: 2021 Mar 3.
Published in final edited form as: Cell Metab. 2020 Feb 6;31(3):580–591.e5. doi: 10.1016/j.cmet.2020.01.009

Figure 6. SIRT2 and NLRP3 deacetylation reverse aging-associated inflammation and insulin resistance.

Figure 6.

(A) Experimental design.

(B, C) Immortalized myeloid progenitors from old WT mice were transduced with control or SIRT2 lentivirus (B), WT or constitutively deacetylated mutant NLRP3 virus (C), selected, differentiated into macrophages, and treated for inflammasome activation. Cell lysates were used for Western analyses for pro IL-1β and pro caspase 1. Culture supernatants were used for p17 IL-1β and p20 caspase 1 Western analyses.

(D, E, F) Macrophages derived from immortalized myeloid progenitors from young or old mice with specified transduction were co-cultured with a piece of intact white adipose tissue from young or old mice as indicated, stimulated for NLRP3 inflammasome activation, followed by insulin signaling activation. The insulin signaling in the white adipose tissues was assessed by Western analyses.