Roles of AQP5/AQP5-G103D in carbamylcholine-induced volume decrease and in reduction of the activation energy for water transport by rat parotid acinar cells
Roles of AQP5/AQP5-G103D in carbamylcholine-induced volume decrease and in reduction of the activation energy for water transport by rat parotid acinar cells
复制标题
AQP5/AQP5-G103D 在氨甲酰胆碱诱导的大鼠腮腺腺泡细胞水运输体积减少和活化能降低中的作用
DOI：
10.1007/s00424-012-1141-8
复制
发表时间：
2012
期刊：
影响因子：
--
通讯作者：
K. Hosoi
中科院分区：
文献类型：
--
作者：
Keitaro Satoh;Yoshiteru Seo;Shinsuke Matsuo;M. Karabasil;M. Matsuki;T. Nakahari;K. Hosoi
为了评估水通道蛋白-5（AQP 5）对唾液腺腺泡细胞水转运的贡献，我们测量了从AQP 5-G103 D突变体及其野生型大鼠获得的分离的腮腺腺泡细胞的细胞体积和扩散水渗透的活化能（Ea）。免疫组化结果显示，在野生型大鼠腺泡细胞中检测到的AQP 5在氨甲酰胆碱（CCh; 1 μM）诱导下没有变化。突变大鼠的腺泡细胞，产生低水平的AQP 5在顶端膜，表现出最小的增加，由于CCh的AQP 5。在野生型大鼠中，CCh引起腺泡短暂肿胀，随后是激动剂诱导的细胞快速收缩，在30 s时达到平台。在突变体大鼠中，腺泡没有膨胀的CCh的挑战，和激动剂诱导的细胞收缩延迟8秒，达到一个短暂的最小值在1分钟左右，并自发恢复，即使CCh是持续存在的。在未受刺激的野生型腺泡细胞中，Ea为3.4 ± 0.6 kcal mol−1，在CCh刺激后没有检测到变化。在未受刺激的突变腺泡细胞中，检测到高Ea值（5.9 ± 0.1 kcal mol−1），并在CCh刺激后显示出极轻微的降低（5.0 ± 0.3 kcal mol−1）。这些结果表明，AQP 5是腺泡细胞中水运输的主要途径，它是负责快速激动剂诱导的腺泡细胞收缩，也有必要保持腺泡细胞体积减少在稳定的分泌在野生型大鼠。
In order to assess the contribution of the water channel aquaporin-5 (AQP5) to water transport by salivary gland acinar cells, we measured the cell volume and activation energy (Ea) of diffusive water permeability in isolated parotid acinar cells obtained from AQP5-G103D mutant and their wild-type rats. Immunohistochemistry showed that there was no change induced by carbamylcholine (CCh; 1 μM) in the AQP5 detected in the acinar cells in the wild-type rat. Acinar cells from mutant rats, producing low levels of AQP5 in the apical membrane, showed a minimal increase in the AQP5 due to the CCh. In the wild-type rat, CCh caused a transient swelling of the acinus, followed by a rapid agonist-induced cell shrinkage, reaching a plateau at 30 s. In the mutant rat, the acinus did not swell by CCh challenge, and the agonist-induced cell shrinkage was delayed by 8 s, reaching a transient minimum at around 1 min, and recovered spontaneously even though CCh was persistently present. In the unstimulated wild-type acinar cells, Ea was 3.4 ± 0.6 kcal mol−1 and showed no detectable change after CCh stimulation. In the unstimulated mutant acinar cells, high Ea value (5.9 ± 0.1 kcal mol−1) was detected and showed a minimal decrease after CCh stimulation (5.0 ± 0.3 kcal mol−1). These results suggested that AQP5 was the main pathway for water transport in the acinar cells and that it was responsible for the rapid agonist-induced acinar cell shrinkage and also necessary to keep the acinar cell volume reduced during the steady secretion in the wild-type rat.
影响因子：
5.5
作者：
Solenov, E;Watanabe, H;Verkman, AS
通讯作者：
Verkman, AS