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首页> 外文期刊>American Journal of Physiology >Mechanisms of Ca2+-stimulated fluid secretion by porcine bronchial submucosal gland serous acinar cells.
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Mechanisms of Ca2+-stimulated fluid secretion by porcine bronchial submucosal gland serous acinar cells.

机译：猪支气管黏膜下腺浆液性腺泡细胞分泌钙离子的机制。

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The serous acini of airway submucosal glands are important for fluid secretion in the lung. Serous cells are also sites of expression of the cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channel. However, the mechanisms of serous cell fluid secretion remain poorly defined. In this study, serous acinar cells were isolated from porcine bronchi and studied using optical techniques previously used to examine fluid secretion in rat parotid and murine nasal acinar cells. When stimulated with the cholinergic agonist carbachol, porcine serous cells shrank by approximately 20% (observed via DIC microscopy) after a profound elevation of intracellular [Ca(2+)] ([Ca(2+)](i); measured by simultaneous fura 2 fluorescence imaging). Upon removal of agonist and relaxation of [Ca(2+)](i) to resting levels, cells swelled back to resting volume. Similar results were observed during stimulation with histamine and ATP, and elevation of [Ca(2+)](i) was found to be necessary and sufficient to activate shrinkage. Cell volume changes were associated with changes in [Cl(-)](i) (measured using SPQ fluorescence), suggesting that shrinkage and swelling are caused by loss and gain of intracellular solute content, respectively, likely reflecting changes in the secretory state of the cells. Shrinkage was inhibited by niflumic acid but not by GlyH-101, suggesting Ca(2+)-activated secretion is mediated by alternative non-CFTR Cl(-) channels, possibly including Ano1 (TMEM16A), expressed on the apical membrane of porcine serous cells. Optimal cell swelling/solute uptake required activity of the Na(+)K(+)2Cl(-) cotransporter and Na(+)/H(+) exchanger, both of which are expressed on the basolateral membrane of serous acini and likely contribute to sustaining transepithelial secretion.
机译：气道粘膜下腺的浆液性腺泡对于肺液分泌很重要。浆液细胞也是囊性纤维化跨膜电导调节剂（CFTR）Cl（-）通道的表达位点。但是，浆液细胞液分泌的机制仍然不清楚。在这项研究中，从猪支气管中分离出浆液腺泡细胞，并使用先前用于检查大鼠腮腺和鼠鼻腺泡细胞中液体分泌的光学技术进行了研究。当用胆碱能激动剂卡巴胆碱刺激时，细胞内[Ca（2+）]（[Ca（2 +）]（i）高度升高后，猪浆液细胞收缩约20％（通过DIC显微镜观察）;同时进行呋喃2荧光成像）。去除激动剂并将[Ca（2 +）]（i）松弛至静止水平后，细胞膨胀回到静止体积。在用组胺和ATP刺激过程中观察到相似的结果，并且发现[Ca（2 +）]（i）升高对于激活收缩是必要和充分的。细胞体积的变化与[Cl（-）]（i）的变化（使用SPQ荧光测量）有关，表明收缩和溶胀分别是由细胞内溶质含量的损失和增加引起的，可能反映了细胞分泌状态的变化。细胞。收缩率受到尼氟酸的抑制，但不受GlyH-101的抑制，表明Ca（2+）激活的分泌是由替代性的非CFTR Cl（-）通道介导的，可能包括猪浆液顶膜上表达的Ano1（TMEM16A）细胞。 Na（+）K（+）2Cl（-）共转运蛋白和Na（+）/ H（+）交换子的最佳细胞溶胀/溶质吸收所需活性，二者均在浆液性腺泡的基底外侧膜上表达，并可能有助于维持上皮分泌。

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