当前位置: X-MOL 学术J. Cell. Mol. Med. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Lin28a up-regulation is associated with the formation of restenosis via promoting proliferation and migration of vascular smooth muscle cells.
Journal of Cellular and Molecular Medicine ( IF 4.3 ) Pub Date : 2020-07-25 , DOI: 10.1111/jcmm.15506
Zhiwei Zou 1, 2 , Xiaojun Zhou 3, 4 , Ruzhen Zhang 4 , Qian Zhang 1, 5, 6 , Shan Jiang 1, 5, 6 , Chunmei Xu 4 , Rui Zhang 1, 5, 6 , Tianyue Xie 3, 4 , Huangao Zhu 1, 5, 6 , Piyun Gong 1, 5, 6 , Dongmei Zhang 1, 5, 6 , Huimei Ma 1, 5, 6 , Lin Liao 3, 4 , Jianjun Dong 1, 5, 6
Affiliation  

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.

中文翻译:

Lin28a的上调通过促进血管平滑肌细胞的增殖和迁移与再狭窄的形成有关。

为了探讨Lin28a在经皮腔内血管成形术后发生再狭窄中的潜在作用,分别采用双气囊损伤手术和单气囊损伤手术分别建立了再狭窄和动脉粥样硬化模型,以便更好地区分再狭窄和动脉粥样硬化病变。免疫组织化学分析显示,在再狭窄斑块的the动脉中观察到的Lin28a表达明显高于动脉粥样硬化斑块。免疫荧光研究表明,Lin28a与α-平滑肌肌动蛋白在再狭窄斑块中而不是在动脉粥样硬化斑块中共定位,这表明Lin28a可能与再狭窄中血管平滑肌细胞(VSMC)的独特行为有关。为了进一步确认上述假设,通过在培养的VSMC中转染Lenti-Lin28a来上调Lin28a的表达,并通过Lenti-Lin28a-shRNA转染来抑制Lin28a的表达,然后分别通过EdU和Transwell分析检测VSMC的增殖和迁移能力。结果表明,随着Lin28a表达的上调,VSMCs的增殖和迁移明显增加,而抑制Lin28a表达后,VSMCs的上述行为被显着抑制。总之,Lin28a的上调对VSMC的增殖和迁移具有调节作用,这可能在促成再狭窄的病理形成中起关键作用。然后分别用EdU和Transwell法检测了VSMC的增殖和迁移能力。结果表明,随着Lin28a表达的上调,VSMCs的增殖和迁移明显增加,而抑制Lin28a表达后,VSMCs的上述行为被显着抑制。总之,Lin28a的上调对VSMC的增殖和迁移具有调节作用,这可能在促成再狭窄的病理形成中起关键作用。然后分别用EdU和Transwell法检测了VSMC的增殖和迁移能力。结果表明,随着Lin28a表达的上调,VSMCs的增殖和迁移明显增加,而抑制Lin28a表达后,VSMCs的上述行为被显着抑制。总之,Lin28a的上调对VSMC的增殖和迁移具有调节作用,这可能在促成再狭窄的病理形成中起关键作用。抑制Lin28a表达后,VSMCs的上述行为得到明显抑制。总之,Lin28a的上调对VSMC的增殖和迁移具有调节作用,这可能在促成再狭窄的病理形成中起关键作用。抑制Lin28a表达后,VSMCs的上述行为得到明显抑制。总之,Lin28a的上调对VSMC的增殖和迁移具有调节作用,这可能在促成再狭窄的病理形成中起关键作用。
更新日期:2020-09-28
down
wechat
bug