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首页> 外文期刊>Cellular Signalling >SH2B1 beta enhances fibroblast growth factor 1 (FGF1)-induced neurite outgrowth through MEK-ERK1/2-STAT3-Egr1 pathway
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SH2B1 beta enhances fibroblast growth factor 1 (FGF1)-induced neurite outgrowth through MEK-ERK1/2-STAT3-Egr1 pathway

机译：SH2B1 beta通过MEK-ERK1 / 2-STAT3-Egr1途径增强成纤维细胞生长因子1（FGF1）诱导的神经突生长

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摘要

Genetic studies have established the crucial roles of FGF signaling, FGF-induced gene expression and morphogenesis during embryogenesis. In this study, we showed that overexpressing a signaling adaptor protein, SH2B1 beta, enhanced FGF1-induced neurite outgrowth in PC12 cells. SH2B1 beta has previously been shown to promote nerve growth factor (NGF) and glial cell line-derived neurotrophic factor (GDNF)-induced neurite outgrowth, in part, through prolonging NGF and GDNF-induced signaling. To delineate how SH2B1 beta promotes FGF1-induced neurite outgrowth, we examined its role in FGF1-dependent signaling. Our data suggest that SH2B1 beta enhances and prolongs FGF1-induced MEK-ERK1/2 and PI3K-AKT pathways. We also provided the first evidence that FGF1 induces the phosphorylation of signal transducer and activator of transcription 3 (STAT3) at serine 727 [pSTAT3(S727)] in PC12 cells. SH2B1 beta enhances this phosphorylation and the expression of the immediate early gene, Egr1. Through inhibitor assays, we have further shown that MEK-ERK1/2 is required for FGF1-induced neurite outgrowth, pSTAT3(5727) and Egr1 expression. Moreover, inhibiting Rho kinase, ROCK, enhances FGF1-induced neurite outgrowth through pSTAT3 (S727)-independent manner. Taken together, our results demonstrate, for the first time, that SH2B1 beta enhances FGF1-induced neurite outgrowth in PC12 cells mainly through MEK-ERK1/2-STAT3-Egr1 pathway.
机译：遗传研究已经确定了FGF信号转导，FGF诱导的基因表达和胚胎发生过程中形态发生的关键作用。在这项研究中，我们表明过表达信号转导蛋白SH2B1 beta增强了PC12细胞中FGF1诱导的神经突增生。 SH2B1 beta以前已被证明可以通过延长NGF和GDNF诱导的信号传导来促进神经生长因子（NGF）和神经胶质细胞系神经营养因子（GDNF）诱导的神经突生长。为了描述SH2B1 beta如何促进FGF1诱导的神经突增生，我们研究了其在FGF1依赖性信号传导中的作用。我们的数据表明，SH2B1 beta增强并延长了FGF1诱导的MEK-ERK1 / 2和PI3K-AKT途径。我们还提供了第一个证据，即FGF1在PC12细胞中诱导丝氨酸727 [pSTAT3（S727）]信号转导和转录激活因子3（STAT3）的磷酸化。 SH2B1 beta增强了这种磷酸化作用，并增强了早期早期基因Egr1的表达。通过抑制剂分析，我们进一步表明，FGF1诱导的神经突增生，pSTAT3（5727）和Egr1表达需要MEK-ERK1 / 2。此外，抑制Rho激酶ROCK通过独立于pSTAT3（S727）的方式增强FGF1诱导的神经突向外生长。两者合计，我们的结果首次证明，SH2B1 beta主要通过MEK-ERK1 / 2-STAT3-Egr1途径增强PC12细胞中FGF1诱导的神经突向外生长。

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