| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1994: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1993: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Research Abstract |
To elucidate the effect of platelet activating factor on mucociliary transport of airway epithelial cells, we studied bioelectric properties of cow tracheal epithelial cells cultured at an airinterface. PAF dose-dependently increased short-circuit current and conductance. This effect was inhibited by Cl channel blocker, DPAC,but not Na channel blocker, amiloride. In addition, this effect was inhibited by the pretreatment of PAF antagonist, BAPTA-AM,and indomethacin, suggesting that PAF increases Cl secretion via PAF receptor, calcium and prostaglandin dependent pathway. Therefore, to elucidate the signal transduction of PAF in the airway epithelial cells, we measured second messengers.
In fura2-loaded cells, PAF increased [Ca^<2+>]i in a dose-dependent manner. This [Ca^<2+>]i response consisted of a transient increase and a subsequent sustained elevation. Ca^<2+>-free medium totally abolished the sustained response, but it only inhibited the transient response. Moreover, PAF increased inositol triphosphate level whose time course was similar to the transient calcium response. PAF also increased PGE2 and PGF2alpha by RIA assay.
These results suggest that PAF-induced epithelial function is mediated by the increased calcium and prostaglandins.
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