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首页> 外文期刊>Molecular reproduction and development >Eomesodermin, HAND1, and CSH1 Proteins Are Induced by Cellular Stress in a Stress-Activated Protein Kinase-Dependent Manner
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Eomesodermin, HAND1, and CSH1 Proteins Are Induced by Cellular Stress in a Stress-Activated Protein Kinase-Dependent Manner

机译：Eomesodermin，HAND1和CSH1蛋白是由细胞应激以应激激活的蛋白激酶依赖性方式诱导的。

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Eomesodermin (Eomes) is a transcription factor essential for trophoblast development. Stress stimuli activate stress-activated protein kinase (MAPK8/9) and modulate transcription factors in trophoblast stem cells (TSC). In this study, we test the hypothesis that stress-induced Eomes upregulation and downstream trophoblast development are MAPK8/9-dependent. Immunocytochemical and immunoblot assays suggest that Eomes is induced by hyperosmolar stress in a dose- and time-dependent manner. Two MAPK8/9 inhibitors that work by different mechanisms, LJNKl1 and SP600125, block induction of Eomes protein by stress. During normal TSC differentiation, the transcription factor heart and neural crest derivatives expressed 1 (HAND1) is dependent on Eomes, and chorionic somatomammotropin hormone 1 (CSH1) expression is dependent on HAND1. Similar to Eomes, HAND1 and CSH1 induction by stress are MAPK8/9-dependent, and CSH1 is induced in nearly all stressed TSC. CSH1 induction normally requires downregulation of the transcription factor inhibitor of differentiation 2 (ID2) as well as HAND1 upregulation. It was shown previously that hyperosmolar stress induces AMP-activated protein kinase (PRKAA1/2)-dependent ID2 loss in a MAPK8/9-independent manner. Inhibition of PRKAA1/2 with compound C and LJNKl1, more than MAPK8/9 inhibitors alone, inhibits the induction of CSH1 by stress. Taken together these data suggest that stress-induced MAPK8/9 and PRKAA1/2 regulate transcription factors Eomes/HAND1 and ID2, respectively. Together this network mediates induction of CSH1 by stress. Therefore, stress triggers a proportional increase in a normal early TSC differentiation event that could be adaptive in inducing CSH1. But the flexibility of TSC to undergo stress-induced differentiation could lead to pathophysiological consequences if stress endured and TSC differentiation became unbalanced. Mol. Reprod. Dev. 78: 519-528, 2011
机译：Eomesodermin（Eomes）是滋养层发育必不可少的转录因子。应激刺激激活了应激激活的蛋白激酶（MAPK8 / 9）并调节了滋养层干细胞（TSC）中的转录因子。在这项研究中，我们测试了以下假设：应激诱导的Eomes上调和下游滋养细胞发育是MAPK8 / 9依赖性的。免疫细胞化学和免疫印迹试验表明，高渗应激可引起Eomes剂量和时间依赖性。两种通过不同机制起作用的MAPK8 / 9抑制剂LJNKl1和SP600125可以通过压力阻止Eomes蛋白的诱导。在正常TSC分化过程中，转录因子心脏和神经rest衍生物1（HAND1）依赖于Eomes，绒毛膜生长激素1（CSH1）的表达依赖于HAND1。与Eomes相似，应激诱导的HAND1和CSH1依赖于MAPK8 / 9，并且几乎所有应激的TSC均诱导CSH1。 CSH1诱导通常需要下调分化2（ID2）转录因子抑制剂以及HAND1上调。先前已证明高渗应激以MAPK8 / 9独立的方式诱导AMP激活的蛋白激酶（PRKAA1 / 2）依赖的ID2丢失。与单独的MAPK8 / 9抑制剂相比，用化合物C和LJNKl1抑制PRKAA1 / 2可以抑制应激诱导的CSH1。这些数据加在一起表明应激诱导的MAPK8 / 9和PRKAA1 / 2分别调节转录因子Eomes / HAND1和ID2。该网络共同通过压力介导CSH1的诱导。因此，压力触发正常的早期TSC分化事件的比例增加，这可能是诱导CSH1的适应性因素。但是，如果压力持续存在且TSC分化变得不平衡，TSC进行应激诱导的分化的灵活性可能会导致病理生理后果。大声笑责备。开发人员78：519-528，2011年

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