Tie1 缺乏可诱导血管内皮-间质转化。
Tie1 deficiency induces endothelial-mesenchymal transition.
机构信息
INSERM U 624, Stress Cellulaire, 163 Avenue de Luminy-Case 915, 13288 Marseille, France.
出版信息
EMBO Rep. 2012 May 1;13(5):431-9. doi: 10.1038/embor.2012.29.
Abstract
Endothelial-mesenchymal transition (EndMT) has a significant role in embryonic heart formation and in various pathologies. However, the molecular mechanisms that regulate EndMT induction remain to be elucidated. We show that suppression of receptor tyrosine kinase Tie1 but not Tie2 induces human endothelial cells to undergo EndMT and that Slug deficiency reverts this process. We find that Erk1/2, Erk5 and Akt cascades control Slug promoter activity induced by Tie1 deficiency. Interestingly, EndMT is present in human pancreatic tumour. We propose that EndMT associated with Tie1 downregulation participates in the pathological development of stroma observed in tumours.
摘要
内皮-间充质转化（EndMT）在胚胎心脏形成和各种病理中起着重要作用。然而，调节 EndMT 诱导的分子机制仍有待阐明。我们表明，抑制受体酪氨酸激酶 Tie1 而不是 Tie2 可诱导人内皮细胞发生 EndMT，而 Slug 缺失可逆转此过程。我们发现 Erk1/2、Erk5 和 Akt 级联控制 Tie1 缺陷诱导的 Slug 启动子活性。有趣的是，EndMT 存在于人类胰腺肿瘤中。我们提出与 Tie1 下调相关的 EndMT 参与了肿瘤中观察到的基质的病理发展。
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