Stimulation of GCMa and syncytin via cAMP mediated PKA signaling in human trophoblastic cells under normoxic and hypoxic conditions
Stimulation of GCMa and syncytin via cAMP mediated PKA signaling in human trophoblastic cells under normoxic and hypoxic conditions
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DOI：
10.1016/j.febslet.2005.06.029
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发表时间：
2005-07-18
期刊：
影响因子：
3.5
通讯作者：
Hashemolhosseini, S
中科院分区：
文献类型：
--
作者：
Knerr, I;Schubert, SW;Hashemolhosseini, S
胶质细胞缺失a （GCMa）是一个新的转录因子家族。合胞素是GCMa的靶基因。在这里，我们证明了蛋白激酶A （PKA）途径作用于GCMa的上游。PKA瞬时转染BeWo细胞后，GCMa的转录活性以及GCMa和合胞素的转录均上调。这种增加伴随着进一步的细胞分化。使用常氧或低氧条件来模拟已知的减少滋养细胞分化的病理生理环境，我们发现缺氧的基因抑制作用通过诱导PKA途径来补偿。我们认为gcma驱动的合胞素表达是合胞滋养细胞形成的关键机制。(c) 2005年由Elsevier B.V.代表欧洲生化学会联合会出版。
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. (c) 2005 Published by Elsevier B.V. on behalf of the Federation of European Biochemical Societies.