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首页> 美国卫生研究院文献>Cells >Authentic and Ectopically Expressed MRGPRX2 Elicit Similar Mechanisms to Stimulate Degranulation of Mast Cells
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Authentic and Ectopically Expressed MRGPRX2 Elicit Similar Mechanisms to Stimulate Degranulation of Mast Cells

机译：正品和异位表达的MRGPRX2引发类似机制以刺激肥大细胞的缩减

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The identification of the Mas-related G-protein-coupled receptors (Mrgpr) as targets of diverse stimuli of mast cells (MCs), including neuropeptides and pseudo-allergy causing drugs, has placed these receptors at a prime position in MC research. However, the species-dependent diversity of these receptors raises the need for an adequate model for investigating the human MRGPRX2 receptor. RBL-2H3 cells, stably transfected with MRGPRX2 (RBL-MRGPRX2), are increasingly used for this purpose. Therefore, we investigated whether ectopically expressed MRGPRX2, in rat MCs, recapitulates its authentic signaling. To this purpose, we performed a broad comparative study of the responses of human LAD-2 MCs that express MRGPRX2 endogenously, and RBL-MRGPRX2 cells to compound 48/80, substance P and vancomycin, three proto-type ligands of MRGPRX2. We demonstrate that both models share similar dose–response relationships, kinetics and sensitivities to a wide range of signaling targeting drugs. Therefore, our results indicate that ectopically expressed MRGPRX2 preserves the signaling pathways employed to evoke human MC degranulation, which we show to rely on ERK1/2 MAP kinases, phospholipase C (PLC) and autophagy-related signaling. Importantly, we also show that the underlying mechanisms of MRGPRX2-triggered MC degranulation in either LAD-2 or RBL-MRGPRX2 cells are different from those elicited by its rodent orthologs.
机译：与MAS相关的G蛋白偶联受体（MRGPR）鉴定为肥大细胞（MCS）的各种刺激的靶标，包括神经肽和伪过敏​​的导致药物，使这些受体处于MC研究中的主要位置。然而，这些受体的物种依赖性多样性提高了需要调查人MRGPRX2受体的足够模型。用MRGPRX2（RBL-MRGPRX2）稳定转染的RBL-2H3细胞越来越多地用于此目的。因此，我们研究了在大鼠MCS中异位表达的MRGPRX2是否重新承认其真实的信令。为此目的，我们对将MRGPRX2的人LAD-2 MCS的反应进行了广泛的比较研究，其表达MRGPRX2和RBL-MRGPRX2细胞化合物48/80，物质P和万古霉素，MRGPRX2的三种原型配体。我们展示两种模型与各种信号传导靶向药物共享相似的剂量 - 响应关系，动力学和敏感性。因此，我们的结果表明，异位表达的MRGPRX2保留了用于引起人MC脱粒的信号传导途径，我们展示依赖于ERK1 / 2映射激酶，磷脂酶C（PLC）和与自噬相关的信号传导。重要的是，我们还表明，LAD-2或RBL-MRGPRX2细胞中MRGPRX2触发MC脱落的潜在机制与其啮齿动物矫形器引起的那些不同的机制。

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