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Sphingosine-1-phosphate promotes mouse melanocyte survival via ERK and Akt activation

机译：鞘氨醇-1-磷酸通过ERK和Akt激活促进小鼠黑素细胞存活

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In this study, we investigated the signalling pathways induced by ultraviolet B (UVB) and the effects of sphingosine-1-phosphate on UVB-induced apoptosis of mouse melanocytes, Mel-Ab, and observed the cytoprotective effects of sphingosine-1-phosphate on UVB-induced apoptosis. Since sphingosine-1-phosphate is a well-known mitogenic agent, we thought it possible that the mitogenic effect of sphingosine-1-phosphate might contribute to cell survival. However, we found that sphingosine-1-phosphate significantly inhibits DNA synthesis. We next examined the regulation of the three major subfamilies of mitogen-activated protein (MAP) kinases and of the Akt pathway by sphingosine-1-phosphate against UVB-induced apoptosis. UVB irradiation resulted in the remarkable and sustained activation of c-Jun N-terminal kinase (INK), while p38 MAP kinase was only transiently activated. The basal level of extracellular signal-regulated protein kinase (ERK) phosphorylation decreased 30 min after UVB irradiation, whereas the basal level of Akt phosphorylation was unaffected by UVB. We also found that sphingosine-1-phosphate potently stimulates the phosphorylation of both ERK and Akt, which are involved in the cell survival-signalling cascade. Furthermore, the specific inhibition of the ERK and Akt pathways by PD98059 and LY294002, respectively, restored the cytoprotective effect induced by sphingosine-1-phosphate. On the other hand, the p38 inhibitor SB203580 additively enhanced the cytoprotective effect on sphingosine-1-phosphate. Based on these results, we conclude that the activation of p38 MAP kinase plays an important role in UVB-induced apoptosis, and that sphingosine-1-phosphate probably exert its cytoprotective effect in Mel-Ab cells through ERK and Akt activation. (C) 2003 Elsevier Science Inc. All rights reserved. [References: 43]
机译：在这项研究中，我们调查了紫外线B（UVB）诱导的信号通路以及鞘氨醇1-磷酸对UVB诱导的小鼠黑素细胞Mel-Ab凋亡的影响，并观察了鞘氨醇1-磷酸对细胞的保护作用。 UVB诱导的细胞凋亡。由于鞘氨醇-1-磷酸是众所周知的促有丝分裂剂，因此我们认为鞘氨醇-1-磷酸的促有丝分裂作用可能有助于细胞存活。但是，我们发现1-磷酸鞘氨醇显着抑制DNA合成。接下来，我们研究了鞘氨醇-1-磷酸针对UVB诱导的细胞凋亡对丝裂原活化蛋白（MAP）激酶和Akt途径的三个主要亚家族的调节。 UVB照射导致c-Jun N端激酶（INK）持续显着活化，而p38 MAP激酶仅被瞬时活化。 UVB照射后30分钟，细胞外信号调节蛋白激酶（ERK）磷酸化的基础水平降低，而Akt磷酸化的基础水平不受UVB的影响。我们还发现，鞘氨醇-1-磷酸可有效刺激ERK和Akt的磷酸化，这与细胞存活信号级联反应有关。此外，PD98059和LY294002分别特异性抑制ERK和Akt途径，恢复了1磷酸鞘氨醇诱导的细胞保护作用。另一方面，p38抑制剂SB203580可额外增强对1-磷酸鞘氨醇的细胞保护作用。基于这些结果，我们得出结论，p38 MAP激酶的激活在UVB诱导的细胞凋亡中起重要作用，而1磷酸鞘氨醇可能通过ERK和Akt激活在Mel-Ab细胞中发挥其细胞保护作用。 （C）2003 Elsevier Science Inc.保留所有权利。 [参考：43]

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