Notch1 signaling induces epithelial-mesenchymal transition in lens epithelium cells during hypoxia.
Notch1 signaling induces epithelial-mesenchymal transition in lens epithelium cells during hypoxia.
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DOI：
10.1186/s12886-017-0532-1
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发表时间：
2017-08-01
影响因子：
2
通讯作者：
Xiao W
中科院分区：
文献类型：
--
作者：
Liu L;Xiao W
后囊膜混浊（PCO）是白内障手术最常见的并发症之一，可导致严重的视力损害。晶状体上皮细胞（LEC）上皮间质转化（EMT）是PCO的病理基础。最近的研究表明，缺氧通过Notch1/Snail1/E-cadherin通路诱导EMT发生。然而，Notch1/Snail1/E-cadherin通路是否参与缺氧下的PCO尚不清楚。观察氯化钴（CoCl2）处理后SRA01/04细胞的形态，采用Western blot和免疫细胞化学方法分析EMT和Notch1/Snail1/E-cadherin通路的标志物。采用Transwell侵袭法和创面愈合法检测转染p3 × FLAG-CMV-7-NICD1对SRA01/04细胞的影响。CoCl2使SRA01/04细胞失去细胞极性和细胞连接。角蛋白、缺氧诱导因子-1α (HIF-1α)、Notch1、snail1表达上调，而纤维连接蛋白、E-cadherin表达下调。Notch1过表达可诱导E-cadherin的表达，增强SRA01/04细胞的侵袭和迁移能力。这些结果表明，Notch1/Snail1/E-cadherin通路通过HIF-1α促进SRA01/04细胞缺氧时的EMT，促进LEC运动。
Posterior Capsular Opacification (PCO) is one of the most common complications of cataract surgery which can result in severe visual damage. Epithelial-Mesenchymal Transition (EMT) of lens epithelium cells (LEC) is the pathological basis of PCO. Recent research showed that hypoxia acted as an inducer of EMT through a Notch1/Snail1/E-cadherin pathway. However, it remains unclear whether the Notch1/Snail1/E-cadherin pathway is involved in PCO under hypoxia. The morphology of SRA01/04 cells treating with Cobalt Chloride (CoCl2) was observed and the markers of EMT and Notch1/Snail1/E-cadherin pathway were analyzed by Western blot and Immunocytochemistry assay. Transwell invasion assay and Wound healing assay were used to detected the effect of p3 × FLAG-CMV-7-NICD1 transfection on the SRA01/04 cells. The SRA01/04 cells lost cell polarity and cell junction culturing with CoCl2. The expression of Keratin, Hypoxia-inducible factor-1 alpha (HIF-1α), Notch1, Snail1were upregulated, on the other side, Fibronectin and E-cadherin were downregulated in hypoxia. Furthermore, the overexpression of Notch1 induced the expression of E-cadherin and increased the invasion and migration ability of SRA01/04 cells. These results suggest that Notch1/Snail1/E-cadherin pathway facilitates the EMT through HIF-1α in SRA01/04 cells during hypoxia and promotes LEC motility.
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