Irie A, Segi E, Sugimoto Y, Ichikawa A, Negishi M
Department of Physiological Chemistry, Faculty of Pharmaceutical Sciences, Kyoto University, Japan.
Biochem Biophys Res Commun. 1994 Oct 14;204(1):303-9. doi: 10.1006/bbrc.1994.2460.
We recently cloned the mouse prostaglandin (PG) E receptor EP3 subtype that is coupled to adenylate cyclase inhibition through Gi and identified three isoforms which are produced through alternative splicing. In Chinese hamster ovary cells expressing each EP3 isoform, PGE2 induced an immediate increase in the intracellular Ca2+ concentration ([Ca2+]i) due to both Ca2+ mobilization from internal stores and influx from the extracellular medium. This increase was abolished by prior treatment with pertussis toxin (PT). PGE2 also stimulated an accumulation of inositol trisphosphate (IP3) in a PT-sensitive manner. Both the PGE2-induced increase in [Ca2+]i and accumulation of IP3 were blocked by the phospholipase C inhibitor U-73122. Thus, EP3 is linked to phospholipase C activation via Gi, and this activation leads to Ca2+ mobilization from internal stores and influx from the extracellular medium.
我们最近克隆了小鼠前列腺素（PG）E受体EP3亚型，该亚型通过Gi与腺苷酸环化酶抑制偶联，并鉴定出通过可变剪接产生的三种异构体。在表达每种EP3异构体的中国仓鼠卵巢细胞中，PGE2导致细胞内Ca2+浓度（[Ca2+]i）立即升高，这是由于Ca2+从内部储存库释放以及从细胞外介质流入所致。这种升高在预先用百日咳毒素（PT）处理后被消除。PGE2还以PT敏感的方式刺激肌醇三磷酸（IP3）的积累。PGE2诱导的[Ca2+]i升高和IP3积累均被磷脂酶C抑制剂U-73122阻断。因此，EP3通过Gi与磷脂酶C激活相关联，并且这种激活导致Ca2+从内部储存库释放以及从细胞外介质流入。
