Fig. 3
The receptor and intracellular mechanisms underlying the potentiation of ASIC3 currents by the activation of PAR2. The a current traces and b bar graphs show that I pH 6.6 was enhanced by PAR2-AP (10−5 M) pre-applied alone for 1 min in CHO cells co-expressing ASIC3 and PAR2. This enhancing effect was inhibited by the co-application of PAR2-AP and FSLLRY-NH2 (10−5 M), a selective PAR2 antagonist. Trypsin, another PAR2 agonist, has a similar increasing effect on I pH 6.6 at concentration of 10−5 M for 1 min. And the enhancing effect of trypsin was also inhibited by FSLLRY-NH2 (10−5 M). Statistical tests were performed using Bonferroni’s post hoc test, and significance is shown as follows: **P < 0.01, compared with white column. n = 10 in each column. The c bar graph shows the percentage increases in the I pH 6.6 induced by PAR2-AP (10−5 M) with recording pipettes filled with the normal internal solution, non-hydrolyzable GDP analog GDP-β-S (500 μM), PLC inhibitor U-73122 (10 μM), PKC inhibitor GF109203X (2 μM), or H-89 (10 μM) containing internal solution. Intracellular dialysis of GDP-β-S, U-73122, GF109203X, or H-89 abolished the enhancing effect of PAR2-AP on I pH 6.6. **P < 0.01, post hoc Bonferroni’s test, compared with normal internal solution. n = 10 in each column