Abstract
Normal human dermal fibroblasts were found to survive and to be active in producing interleukin (IL)-6 and IL-8 under extremely high hydrostatic pressure, up to 40 MPa (1 atm=0.101325 MPa=1.03323 kgf/cm(2)), for 20 min. An inhibitor of protein kinase C (PKC) reduced the amount of IL-6 production, whereas IL-8 production was increased following pressure application. The activation of PKC in response to exposure to the pressure stress was detected by using the PKC-specific probe Rim-1. These findings indicate that IL-6 production induced by hydrostatic pressure stresses was dependent on the PKC signaling pathway. In contrast, pressure-induced IL-8 production was inhibited by PKC activity.
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