Loss of cell polarity regulated by PTEN/Cdc42 enrolled in the process of Hepatopulmonary Syndrome
| العنوان: | Loss of cell polarity regulated by PTEN/Cdc42 enrolled in the process of Hepatopulmonary Syndrome |
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| المؤلفون: | Chang Liu, Bin Yi, Zhiyong Hu, Karine Belguise, Hongfu Yu, Jing Gao, Kaizhi Lu, Lin Chen, Xiaobo Wang, Xue-Hong Bai |
| المصدر: | Journal of Cellular and Molecular Medicine |
| بيانات النشر: | Wiley, 2019. |
| سنة النشر: | 2019 |
| مصطلحات موضوعية: | Male, 0301 basic medicine, PTEN, CDC42, Models, Biological, Vascular remodelling in the embryo, Rats, Sprague-Dawley, Pathogenesis, 03 medical and health sciences, 0302 clinical medicine, Cell Movement, Cell polarity, PMVEC, medicine, Animals, Cdc42, cdc42 GTP-Binding Protein, Hepatopulmonary syndrome, Ligation, Lung, Annexin A2, Cells, Cultured, Cell Proliferation, Common Bile Duct, biology, Cell growth, Chemistry, PTEN Phosphohydrolase, Cell Polarity, Endothelial Cells, Original Articles, Cell Biology, medicine.disease, Cell biology, Actin Cytoskeleton, 030104 developmental biology, 030220 oncology & carcinogenesis, Microvessels, biology.protein, Molecular Medicine, Original Article, Hepatopulmonary Syndrome |
| الوصف: | One central factor in hepatopulmonary syndrome (HPS) pathogenesis is pulmonary vascular remodelling (PVR) which involves dysregulation of proliferation and migration in pulmonary microvascular endothelial cells (PMVECs). Growing evidence suggests that Apical/basolateral polarity plays an important role in cell proliferation, migration, adhesion and differentiation. In this study, we explored whether cell polarity is involved and critical in experimental HPS rats that are induced by common bile duct ligation (CBDL). Cell polarity related proteins were analysed in CBDL rats lung and PMVECs under the HPS serum stimulation by immunofluorescence assay. Cdc42/PTEN activity, cell proliferation and migration and Annexin A2 (AX2) in PMVECs were determined, respectively. Cell polarity related proteins, lost their specialized luminal localization in PMVECs of the CBDL rat. The loss of cell polarity was induced by abnormal activity of Cdc42, which was strongly enhanced by the interaction between p‐PTEN and Annexin A2 in PMVECs, after treatment with serum from CBDL rats. It led to over‐proliferation and high migration ability of PMVECs. Down‐regulation of PTEN‐Cdc42 activity in PMVECs restored cell polarity and thus reduced their ability of migration and proliferation. Our study suggested that the loss of cell polarity plays a critical role in the pathogenesis of HPS‐associated PVR and may become a potentially effective therapeutic target. |
| تدمد: | 1582-4934 1582-1838 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::7181e459259b8b252c06d4bb43ff2738 https://doi.org/10.1111/jcmm.14437 |
| حقوق: | OPEN |
| رقم الأكسشن: | edsair.doi.dedup.....7181e459259b8b252c06d4bb43ff2738 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15824934 15821838 |
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