Abstract

Cholecystokinin 1 receptor (CCK1R) is photodynamically activated permanently by singlet oxygen in rat pancreatic acini or in cell lines ectopically expressing human CCK1R, with light irradiation after exposure to photosensitizer sulphonated aluminium phthalocyanine (SALPC) or miniSOG. It is scientifically important to determine whether this property is evolutionarily conserved. Therefore photodynamic activation of CCK1R in pancreatic acini isolated from rat, mouse, Peking duck, and of CCK1R (or CCK1R‐like receptor) from human, rat, mouse, Peking duck, zebrafish, drosophila, C. elegans expressed in CHO‐K1 cells was examined, as monitored by Fura‐2 fluorescence calcium imaging. SALPC photodynamic action (SALPC 1 μM + LED 675 nm / 40 mW·cm‐2, 1.5 min) was found to trigger persistent calcium oscillations in pancreatic acinar cells isolated from rat, mouse, Peking duck, a hallmark of permanent photodynamic CCK1R activation, as well as in CHO‐K1 cells expressing CCK1R or CCK1R‐like receptor of human, rat, mouse, Peking duck, zebrafish, drosophila, C. elegans origin. Further, miniSOG photodynamic action (miniSOG fused to the C‐terminus of CCK1R + LED 450 nm / 85 mW·cm‐2, 1.5 min) elicited persistent calcium oscillations in CCK1R‐miniSOG‐CHO‐K1 cells, with CCK1R or CCK1R‐like receptor of human, rat, mouse, Peking duck, zebrafish, drosophila, and C. elegans origin. It is concluded therefore that photodynamic CCK1R activation is evolutionarily conserved from worm to human being. Although the structural basis for photodynamic CCK1R activation remains to be elucidated, it is noteworthy that certain critical singlet oxygen‐susceptible residues in CCK1R are conserved among these species.

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