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. 2001 May 1;107(9):1145–1152. doi: 10.1172/JCI12089

Figure 3.

Figure 3

IL-18 in ischemic ARF. (a) IL-18 protein, measured by the ECL assay, was increased in ischemic ARF in wild-type (WT) mice compared with sham-operated controls (sham). AP < 0.01 vs. sham, n = 6. (b) In sham-operated wild-type (WT) and caspase-1–/– mice, IL-18 was predominantly in the pro–IL-18 form (22 kDa). In wild-type mice with ischemic ARF (ARF WT), there was a conversion of the pro–IL-18 form (22 kDa) to the active form (18 kDa). This conversion of the pro–IL-18 to active IL-18 form was attenuated in caspase-1–/– mice with ischemic ARF (ARF–/–). The immunoblot shown is representative of three separate experiments. (c) In an in vitro experiment, cytosolic extracts from normal wild-type WT mouse kidney were incubated with purified caspases. Recombinant murine pro–IL-18 (22 kDa) and active IL-18 (18 kDa) were used as a positive control (Pos) (lane 1). In the cytosolic extract with no additions, IL-18 was present only in the precursor form (lane 2) and addition of purified caspase-3 (10 ng) had no effect (lane 3). Addition of purified caspase-1 (10 ng) completely cleaved IL-18 from the precursor to active form (lane 4) and caspase-1 (1 ng) partially cleaved IL-18 (lane 6). Prior incubation with the caspase inhibitor, Z-VAD-FMK, prevents the cleavage of pro–IL-18 to active IL-18 (lanes 5 and 7). These data demonstrate that caspase-1, but not caspase-3, cleaves IL-18 in the mouse kidney.