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首页> 外文期刊>Journal of Lipid Research >Eicosapentaenoic acid and docosahexaenoic acid modulate MAP kinase (ERK1/ERK2) signaling in human T cells.
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Eicosapentaenoic acid and docosahexaenoic acid modulate MAP kinase (ERK1/ERK2) signaling in human T cells.

机译：二十碳五烯酸和二十二碳六烯酸调节人T细胞中的MAP激酶（ERK1 / ERK2）信号传导。

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This study was conducted on human Jurkat T cell lines to elucidate the role of EPA and DHA, n-3 PUFA, in the modulation of two mitogen-activated protein (MAP) kinases, that is, extracellular signal-regulated kinases 1 and 2 (ERK1 and ERK2). The n-3 PUFA alone failed to induce phosphorylation of ERK1/ERK2. We stimulated the MAP kinase pathway with anti-CD3 antibodies and phorbol 12-myristate 13-acetate (PMA), which act upstream of the MAP kinase (MAPK)/ERK kinase (MEK) as U0126, an MEK inhibitor, abolished the actions of these two agents on MAP kinase activation. EPA and DHA diminished the PMA- and anti-CD3-induced phosphorylation of ERK1/ERK2 in Jurkat T cells. In the present study, PMA acts mainly via protein kinase C (PKC) whereas anti-CD3 antibodies act via PKC-dependent and -independent mechanisms. Furthermore, DHA and EPA inhibited PMA-stimulated PKC enzyme activity. EPA and DHA also significantly curtailed PMA- and ionomycin-stimulated T cell blastogenesis. Together these results suggest that EPA and DHA modulate ERK1/ERK2 activation upstream of MEK via PKC-dependent and -independent pathways and that these actions may be implicated in n-3 PUFA-induced immunosuppression.
机译：这项研究是针对人类Jurkat T细胞系进行的，旨在阐明EPA和DHA n-3 PUFA在调节两种促分裂原活化蛋白（MAP）激酶（即细胞外信号调节激酶1和2）中的作用（ ERK1和ERK2）。单独的n-3 PUFA不能诱导ERK1 / ERK2的磷酸化。我们用抗CD3抗体和佛波醇12-肉豆蔻酸酯13-乙酸酯（PMA）刺激了MAP激酶途径，它们作为MAP抑制剂（U0126）在MAP激酶（MAPK）/ ERK激酶（MEK）的上游起作用，废除了这两种药物对MAP激酶的激活作用。 EPA和DHA减少了Jurkat T细胞中PMA和抗CD3诱导的ERK1 / ERK2磷酸化。在本研究中，PMA主要通过蛋白激酶C（PKC）起作用，而抗CD3抗体则通过PKC依赖性和非依赖性机制起作用。此外，DHA和EPA抑制PMA刺激的PKC酶活性。 EPA和DHA还显着减少了PMA和离子霉素刺激的T细胞的成细胞作用。这些结果共同表明，EPA和DHA通过PKC依赖性和非依赖性途径调节MEK上游的ERK1 / ERK2活化，并且这些作用可能与n-3 PUFA诱导的免疫抑制有关。

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