Schepp W, Steffen B, Schusdziarra V, Classen M
J Clin Endocrinol Metab. 1986 Oct;63(4):886-91. doi: 10.1210/jcem-63-4-886.
We studied prostaglandin E2 (PGE2) release from isolated cells of the human gastric mucosa. Mucosal cells were enzymatically isolated from biopsy specimens of human fundic mucosa. The results from these crude cell preparations were compared to those obtained in fractions with enriched (65-80%) or depleted parietal cell content (3-7%) which were prepared from gastric mucosa obtained at surgery. PGE2 release in the enriched parietal cell fractions exceeded that from crude or parietal cell depleted preparations 3- and 13-fold, respectively. However, despite this quantitative difference, all preparations responded similarly to the test agents. Newly synthesized PGE2 was not stored intracellularly but was released into the incubation medium. Release increased linearly for 30 min. Addition of the calcium ionophore A23187 enhanced PGE2 release 4- to 5-fold. The effect of A23187 required the presence of extracellular Ca2+ (10(-3) mol/liter). Assuming that A23187 alters Ca2+ flux in gastric cells as it does in other cell systems our data indicate that increased Ca2+ influx enhances PGE2 release. Since calmodulin is of importance for intracellular Ca2+ action, the calmodulin antagonists trifluoperazine and W7 were tested. Both antagonists inhibited PGE2 release by 65-85%, trifluoperazine being slightly more effective. Activation of the adenylate cyclase system by forskolin or direct addition of (Bu)2cAMP, a stable cAMP-analog, also inhibited PGE2 release. We conclude that PGE2 is released from parietal and from nonparietal cells of the human gastric mucosa, although the major quantity is released from the light density fraction that is enriched in parietal cells. In parietal and nonparietal cells Ca2+ is of importance in the regulation of gastric mucosal PGE2 release and calmodulin seems to mediate this intracellular action of Ca2+. cAMP inhibits PGE2-release from gastric cells.
我们研究了人胃黏膜分离细胞中前列腺素E2（PGE2）的释放。从人胃底黏膜活检标本中酶法分离黏膜细胞。将这些粗制细胞制剂的结果与从手术获得的胃黏膜制备的富含（65 - 80%）或壁细胞含量减少（3 - 7%）的组分中获得的结果进行比较。富含壁细胞的组分中PGE2的释放分别比粗制制剂和壁细胞减少的制剂高出3倍和13倍。然而，尽管存在这种数量差异，所有制剂对测试剂的反应相似。新合成的PGE2不是储存在细胞内，而是释放到孵育培养基中。释放量在30分钟内呈线性增加。添加钙离子载体A23187可使PGE2释放增加4至5倍。A23187的作用需要细胞外Ca2 +（10（-3）摩尔/升）的存在。假设A23187像在其他细胞系统中一样改变胃细胞中的Ca2 +通量，我们的数据表明增加的Ca2 +内流会增强PGE2的释放。由于钙调蛋白对细胞内Ca2 +的作用很重要，因此测试了钙调蛋白拮抗剂三氟拉嗪和W7。两种拮抗剂均抑制PGE2释放65 - 85%，三氟拉嗪的效果略好。福斯可林激活腺苷酸环化酶系统或直接添加稳定的cAMP类似物（Bu）2cAMP也抑制PGE2释放。我们得出结论，PGE2从人胃黏膜的壁细胞和非壁细胞中释放，尽管主要量是从富含壁细胞的低密度组分中释放。在壁细胞和非壁细胞中，Ca2 +在调节胃黏膜PGE2释放中起重要作用，钙调蛋白似乎介导了Ca2 +的这种细胞内作用。cAMP抑制胃细胞中PGE2的释放。
