دورية أكاديمية
Integrin β3 Mediates the Endothelial-to-Mesenchymal Transition via the Notch Pathway
| العنوان: | Integrin β3 Mediates the Endothelial-to-Mesenchymal Transition via the Notch Pathway |
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| المؤلفون: | Weisen Wang, Zhi Wang, Dingyuan Tian, Xi Zeng, Yangdong Liu, Qining Fu, Anlin Liang, Yi Zhang, Qiangguo Gao, Jizhong Cheng, Yun Wang |
| المصدر: | Cellular Physiology and Biochemistry, Vol 49, Iss 3, Pp 985-997 (2018) |
| بيانات النشر: | Cell Physiol Biochem Press GmbH & Co KG, 2018. |
| سنة النشر: | 2018 |
| المجموعة: | LCC:Physiology LCC:Biochemistry |
| مصطلحات موضوعية: | Integrin β3, endothelial cells, endothelial-to-mesenchymal transition, Notch signaling pathway, neointimal hyperplasia, Physiology, QP1-981, Biochemistry, QD415-436 |
| الوصف: | Background/Aims: Neointimal hyperplasia is responsible for stenosis, which requires corrective vascular surgery, and is also a major morphological feature of many cardiovascular diseases. This hyperplasia involves the endothelial-to-mesenchymal transition (EndMT). We investigated whether integrin β3 can modulate the EndMT, as well as its underlying mechanism. Methods: Integrin β3 was overexpressed or knocked down in human umbilical vein endothelial cells (HUVECs). The expression of endothelial markers and mesenchymal markers was determined by real-time reverse transcription PCR (RT-PCR), immunofluorescence staining, and western blot analysis. Notch signaling pathway components were detected by real-time RT-PCR and western blot analysis. Cell mobility was evaluated by wound-healing, Transwell, and spreading assays. Fibroblast-specific protein 1 (FSP-1) promoter activity was determined by luciferase assay. Results: Transforming growth factor (TGF)-β1 treatment or integrin β3 overexpression significantly promoted the EndMT by downregulating VE-cadherin and CD31 and upregulating smooth muscle actin α and FSP-1 in HUVECs, and by enhancing cell migration. Knockdown of integrin β3 reversed these effects. Notch signaling was activated after TGF-β1 treatment of HUVECs. Knockdown of integrin β3 suppressed TGF-β1-induced Notch activation and expression of the Notch downstream target FSP-1. Conclusion: Integrin β3 may promote the EndMT in HUVECs through activation of the Notch signaling pathway. |
| نوع الوثيقة: | article |
| وصف الملف: | electronic resource |
| اللغة: | English |
| تدمد: | 1015-8987 1421-9778 |
| Relation: | https://www.karger.com/Article/FullText/493229; https://doaj.org/toc/1015-8987; https://doaj.org/toc/1421-9778 |
| DOI: | 10.1159/000493229 |
| URL الوصول: | https://doaj.org/article/bbd55b710f794f909c16389580f1c5aa |
| رقم الأكسشن: | edsdoj.bbd55b710f794f909c16389580f1c5aa |
| قاعدة البيانات: | Directory of Open Access Journals |
Full Text Finder | تدمد: | 10158987 14219778 |
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| DOI: | 10.1159/000493229 |