Knerr Ina, Schnare Markus, Hermann Kathrin, Kausler Susanne, Lehner Manfred, Vogler Tina, Rascher Wolfgang, Meissner Udo
Children and Youth Hospital, University of Erlangen-Nuremberg, Loschgestr. 15, D-91054, Erlangen, Germany.
Apoptosis. 2007 Jan;12(1):37-43. doi: 10.1007/s10495-006-0329-9.
Fusiogenic glycoprotein syncytin-1, expressed in human placenta, is a promising candidate for acquiring a basic knowledge of placental syncytialization. However, its cellular mode of action is unidentified. We investigated whether syncytin-1 may exert influence on apoptotic processes. Therefore, we incubated CHO cells after stable transfection with syncytin-1 (CHO-52) in the presence or absence of staurosporine (STS), a kinase inhibitor well characterized to induce apoptosis. When testing the phenotype of CHO-52 cells, we could demonstrate that the induction of apoptosis by STS was delayed over a period of up to 24 h. Furthermore, the cell death rate was decreased by approx 75% following transfection of syncytin-1 in CHO-52 compared to mock-treated cells. In detail, after 18h of incubation with 500 nM STS, 64 +/- 2% of CHO-52 cells were viable compared to 16 +/- 1% of CHO-mocks, after 24 h 43 +/- 3% vs 5 +/- 2%, respectively. CHO-52 cells exhibited a lower expression of active caspase 3 and anti-apoptotic Bcl-2 was found to be increased in CHO-52 cells at baseline and following STS treatment. Our study provides first evidence that syncytin-1 serves anti-apoptotic function under certain conditions. A lessened activation of caspase 3 and an increased expression of Bcl-2 are possible mechanisms.
在人胎盘中表达的融合性糖蛋白合体滋养层蛋白-1，是获取胎盘合体化基础知识的一个有前景的候选对象。然而，其细胞作用模式尚不清楚。我们研究了合体滋养层蛋白-1是否可能对凋亡过程产生影响。因此，我们在稳定转染合体滋养层蛋白-1（CHO-52）后的CHO细胞中，在存在或不存在星形孢菌素（STS）的情况下进行培养，星形孢菌素是一种已被充分表征可诱导凋亡的激酶抑制剂。在检测CHO-52细胞的表型时，我们可以证明STS诱导的凋亡在长达24小时的时间段内被延迟。此外，与 mock 处理的细胞相比，在CHO-52中转染合体滋养层蛋白-1后细胞死亡率降低了约75%。具体而言，在与500 nM STS孵育18小时后，64±2%的CHO-52细胞存活，而CHO-mock细胞为16±1%；在24小时后，分别为43±3%和5±2%。CHO-52细胞中活性半胱天冬酶3的表达较低，并且发现在基线时以及STS处理后，抗凋亡蛋白Bcl-2在CHO-52细胞中增加。我们的研究提供了首个证据，表明合体滋养层蛋白-1在某些条件下起抗凋亡作用。半胱天冬酶3激活减少和Bcl-2表达增加可能是其机制。
