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. 2019 Dec 23;7:342. doi: 10.3389/fcell.2019.00342

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Copyright © 2019 Gao, Zhang, Wei, Dai, Zhang, Yang, Li and Bai.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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lncRNA MEG3 targets miR-128-3p in neurogenic differentiation from AECs. (A) The expression of MEG3 was analyzed in normal and induced AECs using RT-qPCR. (B) The binding site between MEG3 and miR-128-3p was predicted using bioinformatics algorithms and subsequently mutated to verify interactions. (C) Full-length MEG3 (WT) and sequences containing different mutated variants of the miR-128-3p binding site (MUT) were tested to determine the effect on miR-15/16 expression. The pRL-40 vector alone was used as an internal control. Results are expressed as relative luciferase activity and represent the mean ± SD of at least three replicates. (D) Immunoprecipitation of Myc-tagged Argonaute 2 (AGO2) from AECs co-transfected with Myc-AGO2 and either miR-128-3p or Let-7a (negative control). Empty vector (EV) served as the Myc-AGO2-related negative control. MEG3 and β-actin mRNA levels were quantified using qPCR, and relative immunoprecipitate (IP)/input (cell total RNA) values were plotted. ^∗P < 0.05; ^∗∗P < 0.01.