Abstract
Aberrant proliferation and migration of retinal pigment epithelium (RPE) cells contributes to the pathology of various ocular diseases. miR-27b has been reported to be crucial in the regulation of cell differentiation, proliferation, apoptosis, and migration. However, the role of miR-27b on RPE proliferation and migration remains largely unknown. Here the effect of miR-27b on ARPE-19 cells under platelet-derived growth factor (PDGF)-BB stimulation was explored. In this study, we found that the expression level of miR-27b was significantly reduced in ARPE-19 cells under PDGF-BB stimulation. Ectopic expression of miR-27b remarkably inhibited PDGF-BB-induced proliferation and migration in ARPE-19 cells. Furthermore, bioinformatic analysis and luciferase reporter assay showed that NADPH oxidase 2 (Nox2) was a direct target for miR-27b, and that knockdown of Nox2 expression mimicked the inhibitory effect of miR-27b on PDGF-BB −induced proliferation and migration in ARPE-19 cells, whereas, restoration of Nox2 expression showed an opposite effect. In addition, the ROS production and the activation of P13K/AKT/mTOR signaling induced by PDGF-BB were also suppressed by miR-27b overexpression or Nox2 silencing. Thus, these findings indicated that miR-27b exerted its protective role in RPE cells under PDGF-BB stimulation was partially through regulation of Nox2 and its downstream P13K/AKT/mTOR signaling, which might be a potential therapeutic approach for treatment of diseases caused by RPE proliferation, and migration.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.