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. 2009 Jun 26;297(2):H874–H886. doi: 10.1152/ajpheart.00311.2009

Fig. 6.

Fig. 6.

IL-18 induces EMMPRIN expression in part via reactive oxygen species (ROS) generation. A: IL-18 stimulates ROS generation in SMCs. SMCs were loaded with the fluorophore 2′,7′-dichlorofluorescein (DCF) diacetate (DCFH-DA), then stimulated with IL-18 as indicated, and monitored for up to 15 min in a microplate. DCF fluorescence was normalized to DNA content and represented as fold increase from untreated. *P < 0.05 and **P < 0.001 vs. control at 5 min (n = 12 experiments). B: IL-18-stimulated ROS generation is inhibited by resveratrol and the NADPH oxidase inhibitor diphenyleneiodonium chloride (DPI). SMCs were loaded with DCFH-DA as in A and treated with resveratrol (25 μM in DMSO for 1 h) or DPI (10 μM in DMSO for 30 min), followed by the addition of IL-18 (10 ng/ml). DCF fluorescence was quantified at 5 min. *P < 0.001 vs. untreated; †P < 0.05 and ††P <0.01 vs. IL-18 (n = 12 experiments). C: inhibition of ROS generation blunts IL-18-mediated EMMPRIN expression. SMCs were treated with resveratrol or DPI as in B and then treated with IL-18 (10 ng/ml for 24 h). EMMPRIN mRNA was analyzed by RT-qPCR. *P < 0.001 vs. untreated; †P < 0.05 and ††P <0.001 vs. IL-18 (n = 6 experiments).