抄録
ATP is released from various cells by specific stimulus and cellular damage, and serves as a chemical mediator/transmitter for intercellular signaling. Upon a mechanical stimulus, cultured epidermal keratinocytes release ATP, which is proposed to transmit the mechanical information to sensory nerve terminals in the skin. Because heat-sensitive ion channels, TRPV3 and V4, are expressed in keratinocytes, we hypothesized that heat also causes ATP release from keratinocytes to transmit the thermal signal to neurons or elicit other biological events in the skin. To assess whether heat causes ATP release from the skin, excised mouse scrotal skin was superfused with Krebs-Henseleit solution in a small bath, and ATP concentration in the superfusate was measured by luciferin-luciferase assay. Upon heat application up to ∼42°C, two types of heat-evoked ATP release were observed: one is slowly activated from lower temperature (∼29°C), and another is steeply activated at higher temperature (∼40°C). The latter response only was significantly reduced by ruthenium red (RR, 50 μM), a wide-range inhibitor for TRPs. The RR-sensitive ATP release was activated at near the activation temperature of cultured keratinocytes (Tominaga et al., J. Physiol. Sci., 57, Suppl., S99, 2007). These results support that heat causes ATP release from the skin by the mechanisms involving TRPV3/V4 or other TRPs. ATP might have a role in intercellular signaling of temperature-sensitive events occurring in the skin. [J Physiol Sci. 2008;58 Suppl:S111]
