CAJ | 학술논문

目的：观察2型1－磷酸鞘氨醇受体（ S1PR2）对体外培养的人冠脉内皮细胞增殖的影响。方法：在体外培养的人冠状动脉内皮细胞中，应用 MTT 比色法检测给予1－磷酸鞘氨醇（ S1P ）和 S1PR2特异性拮抗剂 JTE-013处理后内皮细胞增殖情况的改变。结果：1μmol／L S1P 明显促进内皮细胞增殖， S1PR2拮抗剂 JTE-013剂量依赖性抑制 S1P 诱导的内皮细胞增殖。 S1PR2拮抗剂 JTE-013明显抑制内皮细胞中S1P 诱导的p-ERK 磷酸化水平。结论：S1PR2可能通过激活 ERK 信号通路参与 S1P 诱导的内皮细胞增殖过程。
목적：관찰2형1－린산초안순수체（ S1PR2）대체외배양적인관맥내피세포증식적영향。방법：재체외배양적인관상동맥내피세포중，응용 MTT 비색법검측급여1－린산초안순（ S1P ）화 S1PR2특이성길항제 JTE-013처리후내피세포증식정황적개변。결과：1μmol／L S1P 명현촉진내피세포증식， S1PR2길항제 JTE-013제량의뢰성억제 S1P 유도적내피세포증식。 S1PR2길항제 JTE-013명현억제내피세포중S1P 유도적p-ERK 린산화수평。결론：S1PR2가능통과격활 ERK 신호통로삼여 S1P 유도적내피세포증식과정。
Objective To explore the role of sphingosine-1-phosphate receptor (S1PR2) in human coronary artery endothelial cell proliferation in vitro. Methods MTT assay was used to detect cell proliferation in human coronary artery endothelial after treatment of S1P and S1PR2 antagonist JTE-013. Phosphor-ERK and total- ERK level were measured by western blot in endothelial after treatment of S1P and JTE-013. Results 1 μmol/L S1P significantly increased endothelial cells proliferation. S1PR2 antagonist JTE-013 inhibited S1P-induced endothelial cell proliferation in dose-dependent manner. S1PR2 antagonist JTE-013 significantly inhibited S1P-induced phosphor-ERK level in endothelial cells. Conclusion S1PR2 may involve in S1P-induced endothelial cell proliferation through activation of ERK pathway.