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Long-chain fatty acid-induced intracellular signaling in GPR120-expressing brush cells at the limiting ridge of the murine stomach

机译:长链脂肪酸诱导在鼠胃的限制脊的GPR120表达刷细胞中的细胞内信号传导

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摘要

Brush cells at the gastric groove have been proposed to operate as sensory cells capable of sensing constituents of ingested food. Recent studies have indicated that these cells express GPR120 (also known as FFAR4), the G protein-coupled receptor for long-chain fatty acids (LCFAs). However, functional implications of this receptor in brush cells have remained elusive. Here, we show that a great proportion of brush cells express GPR120. We used phosphorylation of the extracellular signal-regulated kinases 1/2 (ERK1/2) as a readout to monitor brush cell responses to the LCFAs oleic acid and -linolenic acid. Our results demonstrate that ERK1/2 phosphorylation is increased upon exposure to both fatty acids. Increased ERK1/2 phosphorylation is accompanied by upregulated mRNA and protein levels of cyclooxygenase 2 (COX-2), a key enzyme for prostaglandin biosynthesis. Immunohistochemical experiments confirmed that oleic acid caused ERK1/2 phosphorylation and induced COX-2 expression in brush cells. Our results indicate that LCFA sensing elicits a signaling process in brush cells that may be relevant for a local regulation of gastric functions.
机译:已经提出了胃槽的刷细胞作为能够感测摄入食物的成分的感觉细胞操作。最近的研究表明,这些细胞表达GPR120(也称为FFAR4),用于长链脂肪酸的G蛋白偶联受体(LCFA)。然而,这种受体在刷细胞中的功能含义仍然难以捉摸。在这里,我们表明大量刷细胞表达GPR120。我们使用细胞外信号调节激酶1/2(ERK1 / 2)的磷酸化作为读出,以监测对LCFA油酸和-LINOLENIC酸的刷细胞应答。我们的结果表明,在暴露于两种脂肪酸后,ERK1 / 2磷酸化增加。增加的ERK1 / 2磷酸化伴随着环氧氧酶2(COX-2)的上调mRNA和蛋白质水平,是前列腺素生物合成的关键酶。免疫组织化学实验证实,油酸引起ERK1 / 2磷酸化和诱导的刷细胞中的COX-2表达。我们的结果表明,LCFA检测引发了刷细胞中的信号传导过程,其可能与胃功能的局部调节相关。

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