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. 2013 Nov 11;54(12):7395–7401. doi: 10.1167/iovs.13-12500

Figure 1.

Figure 1

(A) Two-signal model of the NLRP3 inflammasome is shown: NLRP3 activation requires two signals called “priming” and “activation.” Priming involves induction of inflammasome genes (NLRP3, IL-18, and IL-1β), and activation involves the assembly of a multiprotein scaffold consisting of NLRP3, ASC, and pro-caspase-1, which executes the proteolytic activation of caspase-1. Subsequently, the activated caspase-1 cleaves pro-IL-18 and pro-IL-1β into mature cytokines. Human RPE cells preincubated with vehicle (DMSO) or the NF-κB inhibitor Bay 11-7082 (20 μM) were exposed to Alu RNA via transfection of a plasmid encoding Alu RNA (pAlu) or an empty vector control plasmid (pNull). Alu RNA-induced priming of NLRP3 was assessed by real-time qPCR for (B) NLRP3 mRNA abundance and (C) IL-18 mRNA abundance. n = 3. (D) Protein levels of NLRP3 and IL-18 were induced in human RPE cells exposed to Alu RNA; right panel shows densitometric quantification of the bands on the immunoblot. (E) NF-κB is activated (phospho p65) in human RPE cells exposed to Alu RNA; bar chart shows densitometric quantification of the immunoreactive phospho p65 bands. Gene expression results are expressed as means ± SEM, with P < 0.05 considered statistically significant. n represents the number of experiments from which the data was obtained. Representative immunoblots from 3 independent experiments are shown.