Figure 1. Evidence that the UVR-induced autocrine factor is not α-MSH, and that UVR stimulates PGE₂ synthesis.

A). Tyrosinase activity (represented as percent of controls) is increased in loss-of-function (LOF:1307c) MC1R mutants by UVR (*p<0.005), indicating the presence of an autocrine factor that is not α-MSH stimulates tyrosinase activity in response to UVR. Results are the average of four separate experiments performed on melanocytes cultured from MC1R mutant melanocytes (1307c) and melanocytes with confirmed functional MC1R (1408c) +/− standard error of the mean (SEM).

B) Melanocytes showed a 2-fold increase in levels of PGE₂ in response to UVR, which was inhibited by indomethacin, indicating that COX enzymes are activated by UVR in melanocytes. Differences in PGE₂ were statistically significant between irradiated and sham irradiated cells, and between irradiated cells and cells irradiated in the presence of indomethacin (*p=0.12). Each bar represents the average amount of PGE₂ from 3 independent experiments, +/− SEM, in which each condition was performed in triplicate wells, and in which each experiment was performed using melanocytes cultured from a separate Caucasian donor (n=3).

C) UVR induced the phosphorylation of cPLA₂ and increased levels of cPLA₂ protein in melanocytes. Results are representative of 2 experiments. For each experiment, melanocytes cultured from a separate Caucasian donor were used (n=2).