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首页> 外文期刊>The Journal of Experimental Biology >Activation and nuclear translocation of ERK in response to ligand-dependent and -independent stimuli in liver and gill cells from rainbow trout
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Activation and nuclear translocation of ERK in response to ligand-dependent and -independent stimuli in liver and gill cells from rainbow trout

机译：响应虹鳟鱼肝脏和g细胞中配体依赖性和非依赖性刺激，ERK的活化和核易位

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The mitogen-activated protein kinase ERK is an important signalling molecule involved in the control of cell proliferation, differentiation and cell death, targeting molecules at the cell membrane, in the cytosol, and in the nucleus. This study investigated the activation pattern and subcellular distribution of ERK in liver and gill cells of rainbow trout upon hypo-osmotic shock, addition of epidermal growth factor (EGF) and copper treatment. It further set out to characterize the hypothetical role of nuclear-export signal (NES)-dependent relocation of ERK after nuclear entry and the potential involvement of the ERK activator MEK. Although, in primary hepatocytes, ERK was activated in all conditions in a stimulus-specific manner, it did not accumulate in the nucleus, irrespective of the absence or presence of the inhibitor of NES-dependent export leptomycin B (LB). Similarly, in trout hepatoma cells, where pERK levels increased upon osmotic and mitotic stimulation, but not after toxic insult, no significant nuclear translocation was observed. In a gill cell line, levels of pERK increased after osmotic and mitotic stimulation and showed a decrease during incubation with a toxicant. Again, none of these conditions triggered nuclear accumulation of pERK in the gill cells in the absence of LB, but in contrast to the observation in liver cells, both osmotic and mitotic stimulation caused nuclear accumulation in the presence of the inhibitor. The ERK activator MEK, which possesses a NES-sequence, was apparently not involved in nuclear export, as it did not seem to enter the nucleus. Altogether, ERK is activated in trout cells in a stimulus- and cell type-specific manner, and our data suggest that it acutely acts primarily on cytoplasmic or membrane-situated targets in liver cells, whereas it presumably triggers rapid transcriptional activities in gill cells.
机译：有丝分裂原激活的蛋白激酶ERK是重要的信号分子，参与细胞增殖，分化和细胞死亡的控制，靶向分子在细胞膜，细胞质和细胞核中。本研究研究了低渗性休克，添加表皮生长因子（EGF）和铜处理后虹鳟鱼肝和g细胞中ERK的激活模式和亚细胞分布。它进一步阐明了核进入后依赖于核出口信号（NES）的ERK迁移的假想角色以及ERK活化剂MEK的潜在参与的特征。尽管在原代肝细胞中，ERK在所有条件下均以刺激特异性方式被激活，但无论是否存在NES依赖性出口瘦素B（LB）抑制剂，ERK都不会在细胞核中积累。同样，在鳟鱼肝癌细胞中，pERK水平在渗透和有丝分裂刺激下增加，但在毒性侮辱后没有升高，也没有观察到明显的核易位。在a细胞系中，pERK的水平在渗透和有丝分裂刺激后增加，并在与有毒物质孵育期间降低。同样，在没有LB的情况下，这些条件均未触发triggered细胞中pERK的核积累，但是与在肝细胞中观察到的相反，渗透和有丝分裂刺激均在抑制剂存在下引起核积累。具有NES序列的ERK活化剂MEK显然没有参与核出口，因为它似乎没有进入核。总而言之，ERK在鳟鱼细胞中以特定于刺激物和细胞类型的方式被激活，我们的数据表明，ERK主要对肝细胞中的细胞质或膜定位靶标起急性作用，而它可能触发g细胞的快速转录活性。

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