REGULATION OF WATER TRANSPORT VIA PARACELLULAR PATHWAY BY PHOSPHORYLATION AND DEPHOSPHORYLATION IN SALIVARY GLASNDS

研究了神经激肽a或匹罗卡品诱导的大鼠颌下腺涎液分泌与路西法黄细胞旁转运的关系。神经激肽a或匹罗卡品引起的唾液分泌依赖于细胞内Ca^<2+>浓度的增加，这与路西法黄分泌有关。这些结果表明，Ca^<2+>依赖的磷酸化和/或去磷酸化似乎有助于细胞旁运输。另一方面，胰岛素样生长因子I（IGF-I）在培养的大鼠颌下腺细胞中诱导紧密连接蛋白的表达和定位，提示IGF-I参与维持唾液腺细胞旁通路系统。由于IGF-I的作用被pi3激酶抑制剂抑制，pi3激酶的磷酸化似乎有助于IGF-I的作用。

The relationship between neurokinin A-or pilocarpine-provoked salivary fluid secretion and paracellular transport by using Lucifer Yellow was investigated in perfused rat submandibular gland. Salivary fluid secretion provoked by neurokinin A-or pilocarpine was dependent on the increase in intracellular Ca^<2+> concentrations, which was linked to Lucifer Yellow secretion. These results suggest that Ca^<2+>-dependent phosphorylation and/or dephosphorylation appears to contribute to the paracellular transport. On the other hand, expression and localization of tight junction proteins was induced by insulin-like growth factor I(IGF-I) in cultured rat submandibular gland cells, suggesting that IGF-I contributes to maintenance of the paracellular pathway system in salivary gland. Since the IGF-I effect was inhibited by PI3-kinase inhibitors, phosphorylation by PI3-kinase appears to contribute to the effect of IGF-I.