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首页> 外文期刊>Cytokine >Induction of IL-4 release and upregulated expression of protease activated receptors by GM-CSF in P815 cells.
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Induction of IL-4 release and upregulated expression of protease activated receptors by GM-CSF in P815 cells.

机译：GM-CSF在P815细胞中诱导IL-4释放和蛋白酶激活受体的表达上调。

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GM-CSF has been showed to be able to induce up-regulated receptor and cytokine expression in mast cells in inflammatory conditions. However, little is known of its effects on protease activated receptor (PAR) expression and Th2 cytokine secretion from mast cells. In the present study, we examined potential influence of GM-CSF on mast cell PAR expression and IL-4 and IL-10 release by using flow cytometry analysis, quantitative real time PCR, ELISA and cellular activation of signaling ELISA (CASE) techniques. The results showed that GM-CSF induced up to 3.0-fold increase in IL-4 release from P815 cells, and FSLLRY-NH(2) and trans-cinnamoyl (tc)-YPGKF-NH(2) did not affect GM-CSF induced IL-4 release. GM-CSF reduced tryptase and trypsin induced IL-4 release by up to approximately 55.8% and 70.3%, respectively. GM-CSF elicited the upregulated expression of PAR-1, PAR-2, PAR-3 and PAR-4 mRNAs, but enhanced only PAR-4 protein expression in P815 cells. U0126, PD98059 and LY204002 almost completely abolished GM-CSF induced IL-4 release when they were preincubated with P815 cells for 30 min, indicating ERK and Akt cell signaling pathways may be involved in the event. In conclusion, GM-CSF can stimulate IL-4 release from mast cells through an ERK and Akt cell signaling pathway dependent, but PAR independent mechanism. GM-CSF may serve as a regulator for IL-4 production in mast cells and through which participates in the mast cell related inflammation.
机译：GM-CSF已被证明能够在炎症条件下诱导肥大细胞中受体和细胞因子的表达上调。但是，对其肥大细胞中的蛋白酶激活受体（PAR）表达和Th2细胞因子分泌的影响知之甚少。在本研究中，我们通过使用流式细胞仪分析，定量实时PCR，ELISA和信号激活ELISA（CASE）技术，研究了GM-CSF对肥大细胞PAR表达以及IL-4和IL-10释放的潜在影响。结果表明，GM-CSF诱导从P815细胞中释放的IL-4最多增加3.0倍，并且FSLLRY-NH（2）和反式肉桂酰基（tc）-YPGKF-NH（2）不会影响GM-CSF诱导IL-4释放。 GM-CSF将类胰蛋白酶和胰蛋白酶诱导的IL-4释放分别降低了约55.8％和70.3％。 GM-CSF诱导PAR-1，PAR-2，PAR-3和PAR-4 mRNA的表达上调，但仅增强P815细胞中PAR-4蛋白的表达。当U0126，PD98059和LY204002与P815细胞预孵育30分钟时，它们几乎完全废除了GM-CSF诱导的IL-4释放，表明该事件可能涉及ERK和Akt细胞信号通路。综上所述，GM-CSF可以通过ERK和Akt细胞信号通路依赖性但PAR独立机制刺激肥大细胞中IL-4的释放。 GM-CSF可以作为肥大细胞中IL-4产生的调节剂，并通过它参与肥大细胞相关的炎症。

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