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首页> 外文期刊>Physiological Reports >Cell cycle dependent expression of the CCK2 receptor by gastrointestinal myofibroblasts: putative role in determining cell migration
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Cell cycle dependent expression of the CCK2 receptor by gastrointestinal myofibroblasts: putative role in determining cell migration

机译：胃肠道成肌纤维细胞CCK2受体的细胞周期依赖性表达：在确定细胞迁移中的假定作用

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The well?￠????known action of the gastric hormone gastrin in stimulating gastric acid secretion is mediated by activation of cholecystokinin?￠????2 receptors (CCK2R). The latter are expressed by a variety of cell types suggesting that gastrin is implicated in multiple functions. During wound healing in the stomach CCK2R may be expressed by myofibroblasts. We have now characterized CCK2R expression in cultured myofibroblasts. Immunocytochemistry showed that a relatively small proportion (1?￠????6%) of myofibroblasts expressed the receptor regardless of the region of the gut from which they were derived, or whether from cancer or control tissue. Activation of CCK2R by human heptadecapeptide gastrin (hG17) increased intracellular calcium concentrations in a small subset of myofibroblasts indicating the presence of a functional receptor. Unexpectedly, we found over 80% of cells expressing CCK2R were also labeled with 5?￠????ethynyl?￠????2?￠???2?￠????deoxyuridine (EdU) which is incorporated into DNA during S?￠????phase of the cell cycle. hG17 did not stimulate EdU incorporation but increased migration of both EdU?￠????labeled and unlabelled myofibroblasts; the migratory response was inhibited by a CCK2R antagonist and by an inhibitor of IGF receptor tyrosine kinase; hG17 also increased IGF?￠????2 transcript abundance. The data suggest myofibroblasts express CCK2R in a restricted period of the cell cycle during S?￠????phase, and that gastrin accelerates migration of these cells; it also stimulates migration of adjacent cells probably through paracrine release of IGF. Together with previous findings, the results raise the prospect that gastrin controls the position of dividing myofibroblasts which may be relevant in wound healing and cancer progression in the gastrointestinal tract.
机译：众所周知，胃激素胃泌素在刺激胃酸分泌中的作用是通过激活胆囊收缩素β2受体（CCK2R）来介导的。后者由多种细胞类型表达，提示胃泌素涉及多种功能。在胃伤口愈合期间，肌成纤维细胞可能表达CCK2R。现在，我们已经表征了培养的成纤维细胞中CCK2R的表达。免疫细胞化学表明，成肌纤维母细胞中相对较小的比例（1％〜6％）表达受体，而与它们的来源地，肠道区域，或来自癌症或对照组织无关。人七肽胃泌素（hG17）激活CCK2R会增加一小部分成肌纤维细胞的细胞内钙浓度，表明存在功能性受体。出乎意料的是，我们发现表达CCK2R的细胞中有80％以上也被5′→￠乙炔基→￠→2→2→2→￠→脱氧尿苷（EdU）标记。 DNA在细胞周期的S 1+阶段。 hG17不能刺激EdU的掺入，但是会增加EdUα标记的和未标记的成肌纤维细胞的迁移。 CCK2R拮抗剂和IGF受体酪氨酸激酶抑制剂可抑制迁移反应。 hG17还增加了IGFβ2转录本的丰度。数据表明成肌纤维细胞在S 2+细胞期的有限细胞周期中表达CCK2R，而胃泌素能加速这些细胞的迁移。它也可能通过旁分泌IGF刺激邻近细胞的迁移。与先前的发现一起，结果提出了胃泌素控制分裂成纤维细胞的位置的前景，这可能与胃肠道的伤口愈合和癌症进展有关。

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