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首页> 外文期刊>Clinical and experimental allergy : >Lysophosphatidylserine receptor P2Y10: A G protein‐coupled receptor that mediates eosinophil degranulation
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Lysophosphatidylserine receptor P2Y10: A G protein‐coupled receptor that mediates eosinophil degranulation

机译：溶血磷脂酰丝氨酸受体P2Y10：G蛋白偶联受体介导嗜酸性粒细胞溶液

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Summary Background P2Y10, along with GPR 34 and GPR 174, is a G protein‐coupled receptor that is activated by an endogenous lipid mediator lysophosphatidylserine (Lyso PS ). Its expression pattern and its function are completely unknown. We have previously shown that P2Y10 is one of the highly up‐regulated genes at the late differentiation stage during in?vitro eosinophilopoiesis. Objective We explored the expression and functions of P2Y10 in human cord blood ( CB )‐derived and peripheral blood ( PB ) eosinophils. Methods Real‐time PCR , FACS , Western blot, ELISA , and chemotaxis assays were performed to determine the expression and function of P2Y10. Results As CB cells differentiated towards eosinophils, P2Y10 mRNA and protein were abundantly expressed. P2Y10 was the most highly expressed in the granulocytes from PB , to a lesser extent in monocytes, and least in lymphocytes. Further fractionation of granulocytes revealed that eosinophils express P2Y10 much more strongly than do neutrophils. PB eosinophils solely expressed P2Y10 among the three Lyso PS receptors, while PB neutrophils expressed the three at comparable levels. Lyso PS activated both CB and PB eosinophils to induce a robust ERK phosphorylation. Importantly, Lyso PS was capable of triggering degranulation of ECP in PB eosinophils. This response was significantly reduced by pharmacological inhibitors of TNF ‐alpha‐converting enzyme ( TACE ), epidermal growth factor receptor ( EGFR ), and ERK 1/2, which were known to be required in P2Y10‐mediated signalling pathways. However, Lyso PS had no effect on chemotaxis, differentiation, or eosinophil survival. Conclusions and Clinical Relevance Lyso PS provokes eosinophil degranulation through P2Y10. Therefore, P2Y10 is a potential therapeutic target to control eosinophil‐associated diseases.
机译：发明内容背景P2Y10以及GPR 34和GPR 174是G蛋白偶联受体，其由内源性脂质介体溶血磷苷（LySO PS）激活。其表达式模式及其功能完全未知。我们之前已经表明，P2Y10是在嗜酸性体外嗜酸性血症期间晚分化阶段的高度上调基因之一。目的我们探讨了P2Y10在人脐带血（CB）的表达和功能，嗜酸纤度粒细胞的脐血（CB）和外周血（PB）。方法进行实时PCR，FACS，Western印迹，ELISA和趋化性测定以确定P2Y10的表达和功能。结果作为分化为嗜酸性粒细胞的Cb细胞，P2Y10 mRNA和蛋白质大量表达。 P2Y10是从PB的粒细胞中最高度表达的，在单核细胞中的程度较小，并且至少在淋巴细胞中。粒细胞的进一步分馏显示，嗜酸性粒细胞表达P2Y10比中性粒细胞更强烈。 Pb嗜酸性粒细胞仅在三个LySO PS受体中表达P2Y10，而PB中性粒细胞表达了相当水平的三个。 Lyso PS激活CB和Pb嗜酸铯，以诱导鲁棒ERK磷酸化。重要的是，Lyso PS能够在PB嗜酸铯中引发ECP的升级。通过TNF - α-转换酶（TACE）的药理抑制剂，表皮生长因子受体（EGFR）和ERK 1/2的药物抑制剂显着降低了该响应，并且已知在P2Y10介导的信号传导途径中需要。然而，Lyso PS对趋化性，分化或嗜酸性粒细胞存活没有影响。结论和临床关联Lyso PS通过P2Y10激发嗜酸性粒细胞溶解。因此，P2Y10是控制嗜酸性粒细胞相关疾病的潜在治疗靶标。

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    Hwang S. M.; Kim H. J.; Kim S. M.; Jung Y.; Park S. W.; Chung I. Y.;

  • 作者单位

    Department of Bionano TechnologyHanyang UniversityAnsan Gyeonggi‐do Korea;

    Department of Bionano TechnologyHanyang UniversityAnsan Gyeonggi‐do Korea;

    Department of Bionano TechnologyHanyang UniversityAnsan Gyeonggi‐do Korea;

    Department of MicrobiologyGachon UniversityIncheon Korea;

    Graduate School of MedicineSoonchunhyang University HospitalBucheon Gyeonggi‐do Korea;

    Department of Bionano TechnologyHanyang UniversityAnsan Gyeonggi‐do Korea;

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  • 正文语种 eng
  • 中图分类 医学免疫学;
  • 关键词

    basic immunology; eosinophils; innate immunity;

    机译：基本免疫学;嗜酸性粒细胞;先天免疫力;

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