Krzemiński Patryk
Laboratory of Signal Transduction, Department of Cellular and Molecular Neurobiology, Nencki Institute of Experimental Biology, Warszawa, Poland.
Acta Biochim Pol. 2005;52(4):927-30. Epub 2005 Nov 21.
In this study the contribution of the ERK1/2 pathway to sphingosine-induced death and morphological changes of the actin cytoskeleton in glioma C6 cells was investigated. Surprisingly, the level of ERK1/2 phosphorylation does not change after incubation of cells with sphingosine. Despite this, sphingosine induces rounding and detachment of cells without formation of apoptotic bodies. To shed light on this process, a specific inhibitor of ERK1/2 phosphorylation, U0126, was used. Cells incubated simultaneously with sphingosine and U0126 not only detached, but also exhibited formation of apoptotic-like blebs. These data suggest that during sphingosine-induced glioma C6 cell death apoptotic blebbing is dependent on ERK1/2 signalling and occurs only when ERK1/2 activity is decreased or abolished.
在本研究中,我们探究了ERK1/2信号通路在神经鞘氨醇诱导的胶质瘤C6细胞死亡及肌动蛋白细胞骨架形态变化中的作用。令人惊讶的是,用神经鞘氨醇孵育细胞后,ERK1/2的磷酸化水平并未改变。尽管如此,神经鞘氨醇仍可诱导细胞变圆并脱离,且不形成凋亡小体。为了阐明这一过程,我们使用了ERK1/2磷酸化的特异性抑制剂U0126。同时用神经鞘氨醇和U0126孵育的细胞不仅发生了脱离,还出现了凋亡样小泡的形成。这些数据表明,在神经鞘氨醇诱导的胶质瘤C6细胞死亡过程中,凋亡小泡的形成依赖于ERK1/2信号通路,且仅在ERK1/2活性降低或丧失时发生。