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首页> 外文期刊>American Journal of Physiology >GPR93 activation by protein hydrolysate induces CCK transcription and secretion in STC-1 cells.
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GPR93 activation by protein hydrolysate induces CCK transcription and secretion in STC-1 cells.

机译：蛋白水解产物激活GPR93会在STC-1细胞中诱导CCK转录和分泌。

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摘要

In the intestinal lumen, protein hydrolysate increases the transcription and release of cholecystokinin (CCK) from enteroendocrine cells of the duodenal-jejunal mucosa. Our recent discovery that a G protein-coupled receptor, GPR93, is activated by dietary protein hydrolysate causing induced intracellular calcium-mediated signaling events in intestinal epithelial cells raises a possibility that GPR93 might be involved in the protein hydrolysate induction of CCK expression and/or secretion. Using the enteroendocrine STC-1 cells as a model, the present study demonstrates that increasing expression of GPR93 amplifies the peptone induction of endogenous CCK mRNA levels. A similar increase in CCK transcription, indicated by the luciferase reporter activity driven by an 820-bp CCK promoter, is also observed in response to peptone at a dose as little as 6.25 mg/ml, but not to lysophosphatidic acid (LPA), an agonist of GPR93. We discovered that the upregulation of CCK transcription involves ERK1/2, PKA, and calmodulin-dependent protein kinase-mediated pathways. Additionally, GPR93 activation by peptone induces a response in CCK release at 15 min, which continues over a 2-h period. The cAMP level in STC-1 cells overexpressing GPR93 is induced at a greater extent by peptone than by LPA, suggesting a possible explanation of the different effects of peptone and LPA on CCK transcription and secretion. Our data indicate that GPR93 can contribute to the observed induction of CCK expression and secretion by peptone and provide evidence that G protein-coupled receptors can transduce dietary luminal signals.
机译：在肠腔中，蛋白水解产物增加了胆囊收缩素（CCK）从十二指肠-空肠黏膜肠内分泌细胞的转录和释放。我们最近的发现是，G蛋白偶联受体GPR93被饮食蛋白水解产物激活，引起肠上皮细胞中诱导的细胞内钙介导的信号转导事件，这增加了GPR93可能参与蛋白水解产物诱导CCK表达和/或的可能性。分泌。使用肠内分泌STC-1细胞作为模型，本研究表明GPR93的表达增加会放大内源性CCK mRNA水平的蛋白induction诱导。响应于蛋白25的剂量低至6.25 mg / ml，但未响应溶血磷脂酸（LPA）时，也观察到了由820 bp CCK启动子驱动的萤光素酶报道分子活性引起的CCK转录的类似增加。 GPR93激动剂。我们发现CCK转录的上调涉及ERK1 / 2，PKA和钙调蛋白依赖性蛋白激酶介导的途径。此外，蛋白p激活GPR93会在15分钟时诱导CCK释放，并持续2小时。蛋白p比LPA更大程度地诱导过表达GPR93的STC-1细胞中的cAMP水平，这可能解释了蛋白ept和LPA对CCK转录和分泌的不同影响。我们的数据表明，GPR93可能有助于观察到的蛋白p诱导的CCK表达和分泌，并提供G蛋白偶联受体可以转导饮食内腔信号的证据。

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