当前位置: X-MOL 学术Biol. Chem. › 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.)
LncRNA MALAT1 inhibits hypoxia/reoxygenationinduced human umbilical vein endothelial cell injury via targeting the microRNA-320a/RAC1 axis
Biological Chemistry ( IF 3.7 ) Pub Date : 2020-02-25 , DOI: 10.1515/hsz-2019-0316
Rongrong Zhu 1, 2 , Xiao Hu 1, 2 , Wei Xu 1, 2 , Zhourui Wu 1, 2 , Yanjing Zhu 1, 2 , Yilong Ren 1 , Liming Cheng 1, 2
Affiliation  

Abstract Angiogenesis is believed to protect against hypoxia/reoxygenation (H/R)-induced cell injury. MALAT1 and microRNA-320a (miR-320a) are involved in cancer angiogenesis. To investigate the function of the MALAT1/miR-320a axis in H/R-induced cell injury, human umbilical vein endothelial cell (HUVEC) angiogenesis was detected using the Cell Counting Kit-8 (CCK-8), Transwell migration, cell adhesion and tube formation assays. The expression of MALAT1 and miR-320a was revealed by quantitative reverse transcription polymerase chain reaction (qRT-PCR). The direct binding relationship between miR-320a and MALAT1 was detected by RNA immunoprecipitation (RIP) and dual luciferase reporter assays. The data indicated that H/R induces angiogenesis injury and that the expression of MALAT1 was augmented in H/R-stimulated HUVECs. Overexpression of MALAT1 alleviated H/R-stimulated HUVEC dysfunction, whereas silencing of MALAT1 exerted the opposite effects. MALAT1 also reduced miR-320a levels in HUVECs. Overexpression of miR-320a repressed the function of MALAT1 on H/R-stimulated HUVECs, whereas inhibition of miR-320a exerted the opposite effect. Additionally, miR-320a inhibition alleviated H/R-stimulated HUVEC injury via RAC1. Taken together, this investigation concluded that MALAT1 represses H/R-stimulated HUVEC injury by targeting the miR-320a/RAC1 axis.

中文翻译:

LncRNA MALAT1通过靶向microRNA-320a/RAC1轴抑制缺氧/复氧诱导的人脐静脉内皮细胞损伤

摘要 血管生成被认为可以防止缺氧/复氧 (H/R) 诱导的细胞损伤。MALAT1 和 microRNA-320a (miR-320a) 参与癌症血管生成。为了研究 MALAT1/miR-320a 轴在 H/R 诱导的细胞损伤中的功能,使用 Cell Counting Kit-8 (CCK-8)、Transwell 迁移、细胞粘附检测人脐静脉内皮细胞 (HUVEC) 血管生成和管形成试验。MALAT1 和 miR-320a 的表达通过定量逆转录聚合酶链反应 (qRT-PCR) 揭示。miR-320a 和 MALAT1 之间的直接结合关系通过 RNA 免疫沉淀 (RIP) 和双荧光素酶报告基因检测检测到。数据表明 H/R 诱导血管生成损伤,并且 MALAT1 的表达在 H/R 刺激的 HUVEC 中增加。MALAT1 的过表达减轻了 H/R 刺激的 HUVEC 功能障碍,而 MALAT1 的沉默产生了相反的效果。MALAT1 还降低了 HUVEC 中的 miR-320a 水平。miR-320a 的过表达抑制 MALAT1 对 H/R 刺激的 HUVEC 的功能,而抑制 miR-320a 产生相反的效果。此外,miR-320a 抑制通过 RAC1 减轻了 H/R 刺激的 HUVEC 损伤。总之,这项研究得出结论,MALAT1 通过靶向 miR-320a/RAC1 轴来抑制 H/R 刺激的 HUVEC 损伤。miR-320a 抑制通过 RAC1 减轻了 H/R 刺激的 HUVEC 损伤。总之,这项研究得出结论,MALAT1 通过靶向 miR-320a/RAC1 轴来抑制 H/R 刺激的 HUVEC 损伤。miR-320a 抑制通过 RAC1 减轻了 H/R 刺激的 HUVEC 损伤。总之,这项研究得出结论,MALAT1 通过靶向 miR-320a/RAC1 轴来抑制 H/R 刺激的 HUVEC 损伤。
更新日期:2020-02-25
down
wechat
bug