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. 2017 Feb 27;292(15):6123–6134. doi: 10.1074/jbc.M116.769125

Figure 3.

Figure 3.

Activation of BLT2 causes desensitization of TRPV1-mediated calcium influx. Calcium imaging was performed on DRG cells as in Fig. 1 except that cells were incubated with agonists or antagonists 2 min before LTB4 application. A, LTB4-induced (100 nm) TRPV1 sensitization in absence and presence of the BLT-2 agonist CAY10583 (400 nm). The data are shown as means ± S.E. (n = 50–159; one-way ANOVA; Kruskal-Wallis test; Dunn's multiple comparisons test). ***, p < 0.001. B, BLT2 inhibition increases TRPV1 desensitization induced by high dose of LTB4 (1 μm). LTB4-induced (1 μm) TRPV1 desensitization in absence or presence of the BLT2 antagonist LY255283 (10 μm). The data are shown as means ± S.E. (n = 26–93; one-way ANOVA; Kruskal-Wallis test; Dunn's multiple comparisons test). ***, p < 0.001. C and D, BLT2 activation suppresses TRPV1 sensitization induced by different signaling pathways. Capsaicin-induced TRPV1 activation was sensitized using bradykinin (0.5 μm) (C) or the EP4 agonist ONO-AE-329 (500 nm) (D) in the absence or presence of the BLT2 agonist CAY10583 (400 nm). The data are shown as means ± S.E. (C, n = 47–87; D, n = 52–109; one-way ANOVA; Kruskal-Wallis test, Dunn's multiple comparisons test). *, p < 0.05; **, p < 0.01; ***, p < 0.001.