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. Author manuscript; available in PMC: 2020 Apr 1.
Published in final edited form as: J Leukoc Biol. 2019 Jan 28;105(4):729–740. doi: 10.1002/JLB.3A0818-329RRR

Figure 6. The NMDA-R is not required for the pro-inflammatory response to plasmin.

Figure 6.

BMDMs were pre-treated with MK-801 (1.0 μM) or vehicle for 30 min and then for 3 h with 12 nM enzymatically-active tPA (EA-tPA), EA-tPA and plasminogen (Plg) (200 nM), Plg, or vehicle. Expression of the mRNAs encoding TNFα, IL-1β, IL-6 and CCL2 was determined (mean ± SEM; n = 6; **p<0.01, ***p<0.001, N.S., not statistically significant; one-way ANOVA with Bonferroni’s post hoc test). In separate control experiments (not shown), we demonstrated that the MK-801 blocked the ability of 12 nM EI-tPA to inhibit cytokine expression induced by LPS (0.1 μg/ml).