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首页> 外文期刊>American Journal of Physiology >Protease-activated receptor regulation of Cl- secretion in Calu-3 cells requires prostaglandin release and CFTR activation.
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Protease-activated receptor regulation of Cl- secretion in Calu-3 cells requires prostaglandin release and CFTR activation.

机译：蛋白酶激活的Calu-3细胞中Cl分泌的受体调节需要前列腺素释放和CFTR激活。

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Human lung epithelial (Calu-3) cells were used to investigate the effects of protease-activated receptor (PAR) stimulation on Cl(-) secretion. Quantitative RT-PCR (QRT-PCR) showed that Calu-3 cells express PAR-1, -2, and -3 receptor mRNAs, with PAR-2 mRNA in greatest abundance. Addition of either thrombin or the PAR-2 agonist peptide SLIGRL to the basolateral solution of monolayers mounted in Ussing chambers produced a rapid increase in short-circuit current (I(sc): thrombin, 21 +/- 2 microA; SLIGRL, 83 +/- 22 microA), which returned to baseline within 5 min after stimulation. Pretreatment of monolayers with the cell-permeant Ca(2+)-chelating agent BAPTA-AM (50 microM) abolished the increase in I(sc) produced by SLIGRL. When monolayers were treated with the cyclooxygenase inhibitor indomethacin (10 microM), nearly complete inhibition of both the thrombin- and SLIGRL-stimulated I(sc) was observed. In addition, basolateral treatment with the PGE(2) receptor antagonist AH-6809 (25 microM) significantly inhibited the effects of SLIGRL on I(sc). QRT-PCR revealed that Calu-3 cells express mRNAs for CFTR, the Ca(2+)-activated KCNN4 K(+) channel, and the KCNQ1 K(+) channel subunit, which, in association with KCNE3, is known to be regulated by cAMP. Stimulation with SLIGRL produced an increase in apical Cl(-) conductance that was blocked in cells expressing short hairpin RNAs designed to target CFTR. These results support the conclusion that PAR stimulation of Cl(-) secretion occurs by an indirect mechanism involving the synthesis and release of prostaglandins. In addition, PAR-stimulated Cl(-) secretion requires activation of CFTR and at least two distinct K(+) channels located in the basolateral membrane.
机译：人类肺上皮（Calu-3）细胞用于研究蛋白酶激活受体（PAR）刺激对Cl（-）分泌的影响。定量RT-PCR（QRT-PCR）显示Calu-3细胞表达PAR-1，-2和-3受体mRNA，其中PAR-2 mRNA最丰富。将凝血酶或PAR-2激动剂肽SLIGRL添加到安装在Usssings室中的单层基底外侧溶液中，会导致短路电流快速增加（I（sc）：凝血酶，21 +/- 2 microA; SLIGRL，83 + /-22 microA），在刺激后5分钟内恢复到基线。单层细胞渗透性Ca（2 +）-螯合剂BAPTA-AM（50 microM）的预处理消除了SLIGRL产生的I（sc）的增加。当用环氧合酶抑制剂吲哚美辛（10 microM）处理单分子层时，观察到凝血酶和SLIGRL刺激的I（sc）几乎完全被抑制。此外，PGE（2）受体拮抗剂AH-6809（25 microM）的基底外侧治疗显着抑制了SLIGRL对I（sc）的作用。 QRT-PCR显示，Calu-3细胞表达CFTR，Ca（2+）激活的KCNN4 K（+）通道和KCNQ1 K（+）通道亚基的mRNA，与KCNE3关联的是由cAMP调节。用SLIGRL刺激产生的根尖Cl（-）电导增加，在表达针对CFTR的短发夹RNA的细胞中被阻断。这些结果支持这样的结论：PAR刺激Cl（-）分泌是通过涉及前列腺素合成和释放的间接机制发生的。此外，PAR刺激的Cl（-）分泌需要激活CFTR和位于基底外侧膜中的至少两个不同的K（+）通道。

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