Startseite LncRNA MALAT1 inhibits hypoxia/reoxygenation-induced human umbilical vein endothelial cell injury via targeting the microRNA-320a/RAC1 axis
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LncRNA MALAT1 inhibits hypoxia/reoxygenation-induced human umbilical vein endothelial cell injury via targeting the microRNA-320a/RAC1 axis

  • Rongrong Zhu EMAIL logo , Xiao Hu , Wei Xu , Zhourui Wu , Yanjing Zhu , Yilong Ren und Liming Cheng EMAIL logo
Veröffentlicht/Copyright: 13. August 2019

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.

Award Identifier / Grant number: 2016YFA0100800

Award Identifier / Grant number: 81810001048

Award Identifier / Grant number: 81873994

Award Identifier / Grant number: 81671105

Funding statement: This work was financially supported by the National Key Research and Development Program (Grant No. 2016YFA0100800), the Major International (Regional) Joint Research Project (Grant No. 81810001048), and the National Natural Science Foundation of China, (Grant Nos. 81873994 and 81671105).

  1. Conflict of interest statement: The authors do not declare any conflicts of interest.

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Received: 2019-06-06
Accepted: 2019-08-02
Published Online: 2019-08-13
Published in Print: 2020-02-25

©2020 Walter de Gruyter GmbH, Berlin/Boston

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