Laboratory of Pharmacoinformatics, Graduate School of Ritsumeikan University, Kusatsu, Shiga 525-8577, Japan.
Biochem Biophys Res Commun. 2013 Jan 4;430(1):190-5. doi: 10.1016/j.bbrc.2012.11.046. Epub 2012 Nov 23.
We established cell lines that stably express orphan GPCR GPR174 using CHO cells, and studied physiological and pharmacological features of the receptor. GPR174-expressing cells showed cell-cell adhesion with localization of actin filaments to cell membrane, and revealed significant delay of cell proliferation. Since the morphological changes of GPR174-cells were very similar to mock CHO cells treated with cholera toxin, we measured the concentration of intracellular cAMP. The results showed the concentration was significantly elevated in GPR174-cells. By measuring intracellular cAMP concentration in GPR174-cells, we screened lipids and nucleotides to identify ligands for GPR174. We found that lysophosphatidylserine (LysoPS) stimulated increase in intracellular cAMP in a dose-dependent manner. Moreover, phosphorylation of Erk was elevated by LysoPS in GPR174 cells. These LysoPS responses were inhibited by NF449, an inhibitor of Gα(s) protein. These results suggested that GPR174 was a putative LysoPS receptor conjugating with Gα(s), and its expression induced morphological changes in CHO cells by constitutively activating adenylyl cycles accompanied with cell conjunctions and delay of proliferation.
我们利用 CHO 细胞建立了稳定表达孤儿 GPCR GPR174 的细胞系,并研究了该受体的生理和药理学特征。表达 GPR174 的细胞表现出细胞间黏附,肌动蛋白丝定位于细胞膜,并显示出细胞增殖的显著延迟。由于 GPR174 细胞的形态变化与用霍乱毒素处理的 mock CHO 细胞非常相似,我们测量了细胞内 cAMP 的浓度。结果表明,GPR174 细胞中的浓度显著升高。通过测量 GPR174 细胞中的细胞内 cAMP 浓度,我们筛选了脂质和核苷酸,以鉴定 GPR174 的配体。我们发现溶血磷脂酰丝氨酸(LysoPS)以剂量依赖的方式刺激细胞内 cAMP 的增加。此外,LysoPS 在 GPR174 细胞中升高了 Erk 的磷酸化。这些 LysoPS 反应被 NF449 抑制,NF449 是 Gα(s)蛋白的抑制剂。这些结果表明,GPR174 是一种假定的 LysoPS 受体,与 Gα(s)结合,其表达通过组成性激活腺苷酸环化酶诱导 CHO 细胞的形态变化,伴随细胞连接和增殖延迟。