Knerr Ina, Schubert Steffen W, Wich Christina, Amann Kerstin, Aigner Thomas, Vogler Tina, Jung Ronny, Dötsch Jörg, Rascher Wolfgang, Hashemolhosseini Said
University Hospital for Children and Adolescents, University of Erlangen-Nuremberg, Germany.
FEBS Lett. 2005 Jul 18;579(18):3991-8. doi: 10.1016/j.febslet.2005.06.029.
Glial cells missing a (GCMa) belongs to a new transcription factor family. Syncytin was shown to be a target gene of GCMa. Here, we demonstrate that the protein kinase A (PKA) pathway acts upstream of GCMa. After transient transfection of BeWo cells with PKA, GCMa transcriptional activity and both GCMa and syncytin transcripts were upregulated. This increase was accompanied by further cellular differentiation. Using normoxic or hypoxic conditions to mimic pathophysiological settings known to diminish trophoblast differentiation, we found that gene repressive effects of oxygen deficiency were compensated by the induction of the PKA pathway. We propose that GCMa-driven syncytin expression is the key mechanism for syncytiotrophoblast formation.
神经胶质细胞缺失蛋白a（GCMa）属于一个新的转录因子家族。合体素被证明是GCMa的一个靶基因。在此，我们证明蛋白激酶A（PKA）通路在GCMa的上游起作用。用PKA瞬时转染BeWo细胞后，GCMa转录活性以及GCMa和合体素转录本均上调。这种增加伴随着进一步的细胞分化。利用常氧或缺氧条件模拟已知会减少滋养层细胞分化的病理生理环境，我们发现缺氧的基因抑制作用可通过PKA通路的诱导得到补偿。我们提出，GCMa驱动的合体素表达是合体滋养层细胞形成的关键机制。
