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

Fig. 4.

Fig. 4.

IL-18 stimulates EMMPRIN expression via PI3K-Akt-ERK signaling. A: IL-18 induces ERK activation. Quiescent SMCs were incubated with IL-18 (10 ng/ml) for up to 2 h. Cleared cell lysates were immunoblotted with pERK or ERK antibodies (n = 3 experiments). B: IL-18 stimulates ERK activity. Quiescent SMC treated as in A were analyzed for ERK activity using immunecomplex kinase assays. E-26-like protein (Elk) served as a substrate (n = 3 experiments). α-Tubulin served as a control. C: PD-98059 blocks IL-18-mediated ERK activity. Quiescent SMCs treated with PD-98059 (10 μM in DMSO for 1 h) before IL-18 addition were analyzed for ERK activity as described in B (n = 3 experiments). D: adenoviral transduction of dnAkt inhibits IL-18-mediated ERK activity. SMCs transduced with Ad.dnAkt (100 MOI for 24 h) and then treated with IL-18 (10 ng/ml for 1 h) were analyzed for ERK activity as described in B (n = 3 experiments). E: adenoviral transduction of dnPI3Kp85 inhibits IL-18-mediated ERK activity. SMCs transduced with Ad.dnPI3Kp85 (100 MOI for 24 h) and then treated with IL-18 (10 ng/ml for 1 h) were analyzed for ERK activity as described in B (n = 3 experiments). F: IL-18 induces EMMPRIN mRNA expression via PI3K, Akt, and ERK, but not via JNK. SMCs were transduced with Ad.dnPI3K, dnAkt, or dnJNK or treated with PD-98059 before IL-18 addition (10 ng/ml for 24 h). EMMPRIN mRNA expression was analyzed by RT-quantitative (q)PCR (F; n = 6 experiments) or Northern blot analysis (G, H, and I; n = 3 experiments). *P < 0.001 vs. untreated; †P < at least 0.05 vs. IL-18.