Lin28a up‐regulation is associated with the formation of restenosis via promoting proliferation and migration of vascular smooth muscle cells
| Autor: | Shan Jiang, Huimei Ma, Dongmei Zhang, Tianyue Xie, Ruzhen Zhang, Lin Liao, Huangao Zhu, Jianjun Dong, Rui Zhang, Chunmei Xu, Zhiwei Zou, Piyun Gong, Qian Zhang, Xiaojun Zhou |
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| Rok vydání: | 2020 |
| Předmět: |
Male
0301 basic medicine Vascular smooth muscle proliferation Myocytes Smooth Muscle Transfection migration percutaneous transluminal angioplasty Immunofluorescence Muscle Smooth Vascular Rats Sprague-Dawley Lin28a restenosis 03 medical and health sciences 0302 clinical medicine Downregulation and upregulation Restenosis Cell Movement medicine Animals vascular smooth muscle cells Pathological Cells Cultured Cell Proliferation medicine.diagnostic_test business.industry Angioplasty RNA-Binding Proteins Colocalization Original Articles Cell Biology Atherosclerosis medicine.disease Plaque Atherosclerotic Rats Up-Regulation 030104 developmental biology 030220 oncology & carcinogenesis Cancer research Molecular Medicine Immunohistochemistry Original Article business |
| Zdroj: | Journal of Cellular and Molecular Medicine |
| ISSN: | 1582-4934 1582-1838 |
| DOI: | 10.1111/jcmm.15506 |
| Popis: | To explore the potential role of Lin28a in the development of restenosis after percutaneous transluminal angioplasty, double‐balloon injury surgery and mono‐balloon injury surgery were used to establish restenosis and atherosclerosis models, respectively, so as to better distinguish restenosis from atherosclerotic lesions. Immunohistochemical analysis revealed that significantly higher expression of Lin28a was observed in the iliac arteries of restenosis plaques than that of atherosclerosis plaques. Immunofluorescence studies showed the colocalization of Lin28a with α‐smooth muscle actin in restenosis plaques, rather than in atherosclerosis plaques, which suggested that Lin28a might be related to the unique behaviour of vascular smooth muscle cells (VSMCs) in restenosis. To further confirm above hypothesis, Lin28a expression was up‐regulated by transfection of Lenti‐Lin28a and inhibited by Lenti‐Lin28a‐shRNA transfection in cultured VSMCs, and then the proliferation and migration capability of VSMCs were detected by EdU and Transwell assays, respectively. Results showed that the proliferation and migration of VSMCs were significantly increased in accordance with the up‐regulation of Lin28a expression, while above behaviours of VSMCs were significantly suppressed after inhibiting the expression of Lin28a. In conclusion, the up‐regulation of Lin28a exerts its modulatory effect on VSMCs’ proliferation and migration, which may play a critical role in contributing to pathological formation of restenosis. |
| Databáze: | OpenAIRE |
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