首页> 外文期刊>Life sciences >5-HT activates ERK MAP kinase in cultured-human peripheral blood mononuclear cells via 5-HT(1A) receptors.
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5-HT activates ERK MAP kinase in cultured-human peripheral blood mononuclear cells via 5-HT(1A) receptors.

机译:5-HT通过5-HT(1A)受体激活人类外周血单个核细胞中的ERK MAP激酶。

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In the present work, we tested the hypothesis that serotonin (5-hydroxytryptamine = 5-HT) might activate the extracellular signal-regulated kinase (ERK) pathway in human peripheral blood mononuclear cells (PBMC). PBMC were maintained in culture for 72 hrs at 37 degrees C prior to the addition of 5-HT. Our results showed an increase in ERK activation by 5-HT with a peak effect at 30 min and maximal stimulation with 5-HT at 1muM. This activation of ERK did not occur in adherent monocytes suggesting that the effect was on lymphocytes. In addition, p38 MAP kinase was not activated under these conditions. The effect of 5-HT on ERK activation appeared to be mediated through the activation of 5-HT(1A) receptors since similar results were obtained with R-(+)-8-hydroxy-DPAT, a selective 5-HT(1A) receptor agonist and WAY100635, a selective 5-HT(1A) receptor antagonist, reversed the 5-HT and the R-(+)-8-hydroxy-DPAT effects. Results from Western blot analysis confirmed the presence of 5-HT(1A) receptors on the PBMC. A 5-HT(2A) antagonist, ketanserin, and a 5-HT transport inhibitor, fluoxetine, both failed to block the activation of ERK by 5-HT. Our results indicate that 5-HT activates ERK, but not p38, MAP kinase of human PBMC via a 5-HT(1A) receptor.
机译:在目前的工作中,我们测试了5-羟色胺(5-羟色胺= 5-HT)可能激活人外周血单核细胞(PBMC)中细胞外信号调节激酶(ERK)通路的假说。在添加5-HT之前,将PBMC在37℃下培养72小时。我们的研究结果表明,5-HT激活ERK的作用增强,在30分钟时达到峰值,而1μM处的5-HT刺激最大。在粘附的单核细胞中未发生这种ERK激活,表明该作用是对淋巴细胞的。另外,在这些条件下p38 MAP激酶没有被激活。 5-HT对ERK激活的影响似乎是通过激活5-HT(1A)受体来介导的,因为使用R-(+)-8-hydroxy-DPAT,选择性5-HT(1A)获得了相似的结果受体激动剂和WAY100635,选择性的5-HT(1A)受体拮抗剂,逆转了5-HT和R-(+)-8-羟基-DPAT的作用。 Western印迹分析的结果证实了PBMC上存在5-HT(1A)受体。 5-HT(2A)拮抗剂,酮色林和5-HT转运抑制剂氟西汀均不能阻止5-HT激活ERK。我们的结果表明,5-HT通过5-HT(1A)受体激活人PBMC的ERK,但不激活p38 MAP激酶。

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