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首页> 外文期刊>Journal of Cellular Physiology >Cdk5 mediates vimentin Ser56 phosphorylation during GTP-induced secretion by neutrophils.
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Cdk5 mediates vimentin Ser56 phosphorylation during GTP-induced secretion by neutrophils.

机译：Cdk5调节波形蛋白Ser56磷酸化中性粒细胞在GTP-induced分泌。

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Secretion by neutrophils contributes to acute inflammation following injury or infection. Vimentin has been shown to be important for secretion by neutrophils but little is known about its dynamics during secretion, which is regulated by cyclin-dependent kinase 5 (Cdk5). In this study, we sought to examine the vimentin dynamics and its potential regulation by Cdk5 during neutrophil secretion. We show that vimentin is a Cdk5 substrate that is specifically phosphorylated at Ser56. In response to neutrophil stimulation with GTP, vimentin Ser56 was phosphorylated and colocalized with Cdk5 in the cytoplasmic compartment. Vimentin pSer56 and Cdk5 colocalization was consistent with coimmunoprecipitation from stimulated cells. Vimentin Ser56 phosphorylation occurred immediately after stimulation, and a remarkable increase in phosphorylation was noted later in the secretory process. Decreased GTP-induced vimentin Ser56 phosphorylation and secretion resulted from inhibition of Cdk5 activity by roscovitine or olomoucine or by depletion of Cdk5 by siRNA, suggesting that GTP-induced Cdk5-mediated vimentin Ser56 phosphorylation may be related to GTP-induced Cdk5-mediated secretion by neutrophils. Indeed, inhibition of vimentin Ser56 phosphorylation led to a corresponding inhibition of GTP-induced secretion, indicating a link between these two events. While fMLP also induced vimentin Ser56 phosphorylation, such phosphorylation was unaffected by roscovitine, which nonetheless, inhibited secretion, suggesting that Cdk5 regulates fMLP-induced secretion via a mechanism independent of Cdk5-mediated vimentin Ser56 phosphorylation. These findings demonstrate the distinct involvement of Cdk5 in GTP- and fMLP-induced secretion by neutrophils, and support the notion that specific targeting of Cdk5 may serve to inhibit the neutrophil secretory process.
机译：由中性粒细胞分泌导致急性受伤后的炎症或感染。波形蛋白已被证明是重要的中性粒细胞分泌,但所知甚少对其动力学在分泌,这是受细胞周期蛋白依赖性激酶5 (Cdk5)。这项研究中,我们试图检查波形蛋白Cdk5动力学及其潜在的监管在中性粒细胞分泌。波形蛋白是一个专门Cdk5衬底在Ser56磷酸化。中性粒细胞刺激与三磷酸鸟苷,波形蛋白Ser56是磷酸化和与Cdk5细胞质隔间。Cdk5 colocalization是一致的coimmunoprecipitation从刺激细胞。波形蛋白Ser56磷酸化发生后立即刺激,引人注目增加磷酸化后来指出分泌过程。波形蛋白Ser56磷酸化和分泌从抑制Cdk5活动造成的roscovitine或olomoucine Cdk5的损耗核,这表明GTP-inducedCdk5-mediated波形蛋白Ser56磷酸化有关GTP-induced Cdk5-mediated分泌中性粒细胞。Ser56磷酸化导致相应抑制GTP-induced分泌,指示这两个事件之间的联系。波形蛋白诱导Ser56磷酸化,等磷酸化被roscovitine不受影响,尽管如此,抑制分泌,这表明Cdk5调节fMLP-induced分泌通过一个独立的机制Cdk5-mediated波形蛋白Ser56磷酸化。这些发现证明了不同Cdk5参与三磷酸鸟苷和fMLP-induced由中性粒细胞分泌,并支持这一概念Cdk5或许的特定目标抑制中性粒细胞分泌过程。

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