Addition of PM (100 μg/ml) to human lung microvascular ECs produced slow time-dependent Ca 2+ influx ( Figure 3A ; Ca 2+ influx is represented by an increase in the 340/380 ratio of Fura-2 AM.). Notably, this finding of increased intracellular Ca 2+ is in accordance with our previous finding of increased activated calpain. Under oxidative stress, a key member of the transient receptor potential (TRP) cation channel, member M2 (TRPM2), is activated and causes slow calcium influx [22] . We therefore examined the role of activated TRPM2 in PM-stimulated calcium influx. Anti-TRPM2 blocking antibody (5 μg/ml, 4 hr pretreatment) significantly prevented the PM-induced Ca 2+ transients compared to ECs treated with control IgG ( Figure 3B ). Reductions in TRPM2 protein expression (by siRNA) also inhibited the PM-induced Ca 2+ influx compared to ECs treated with control siRNA ( Figure 3C ).