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首页> 外文期刊>American Journal of Physiology >Degradation of extracellular ATP by the retinal pigment epithelium.
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Degradation of extracellular ATP by the retinal pigment epithelium.

机译：视网膜色素上皮降解细胞外ATP。

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Stimulation of ATP or adenosine receptors causes important physiological changes in retinal pigment epithelial (RPE) cells that may influence their relationship to the adjacent photoreceptors. While RPE cells have been shown to release ATP, the regulation of extracellular ATP levels and the production of dephosphorylated purines is not clear. This study examined the degradation of ATP by RPE cells and the physiological effects of the adenosine diphosphate (ADP) that result. ATP was readily broken down by both cultured human ARPE-19 cells and the apical membrane of fresh bovine RPE cells. The compounds ARL67156 and betagamma-mATP inhibited this degradation in both cell types. RT-PCR analysis of ARPE-19 cells found mRNA message for multiple extracellular degradative enzymes; ectonucleotide pyrophosphatase/phosphodiesterase eNPP1, eNPP2, and eNPP3; the ectoATPase ectonucleoside triphosphate diphosphohydrolase NTPDase2, NTPDase3, and some message for NTPDase1. Considerable levels of ADP bathed RPE cells, consistent with a role for NTPDase2. ADP and ATP increased levels of intracellular Ca(2+). Both responses were inhibited by thapsigargin and P2Y(1) receptor inhibitor MRS 2179. Message for both P2Y(1) and P2Y(12) receptors was detected in ARPE-19 cells. These results suggest that extracellular degradation of ATP in subretinal space can result in the production of ADP. This ADP can stimulate P2Y receptors and augment Ca(2+) signaling in the RPE.
机译：ATP或腺苷受体的刺激会引起视网膜色素上皮（RPE）细胞发生重要的生理变化，从而可能影响它们与相邻感光细胞的关系。尽管已显示RPE细胞释放ATP，但尚不清楚细胞外ATP水平的调节和去磷酸化嘌呤的产生。这项研究检查了RPE细胞对ATP的降解以及由此产生的二磷酸腺苷（ADP）的生理作用。培养的人ARPE-19细胞和新鲜牛RPE细胞的顶膜都容易分解ATP。化合物ARL67156和betagamma-mATP在两种细胞类型中均抑制了这种降解。对ARPE-19细胞的RT-PCR分析发现了多种细胞外降解酶的mRNA信息。外核苷酸焦磷酸酶/磷酸二酯酶eNPP1，eNPP2和eNPP3; ectoATPase外核苷三磷酸二磷酸水解酶NTPDase2，NTPDase3，以及一些有关NTPDase1的信息。相当数量的ADP浸泡RPE细胞，与NTPDase2的作用一致。 ADP和ATP增加了细胞内Ca（2+）的水平。毒胡萝卜素和P2Y（1）受体抑制剂MRS 2179均抑制了这两种反应。在ARPE-19细胞中检测到P2Y（1）和P2Y（12）受体的信息。这些结果表明视网膜下空间中ATP的细胞外降解可导致ADP的产生。此ADP可以刺激RPE中的P2Y受体并增强Ca（2+）信号传导。

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