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. 2017 Jun 27;16(3):2522–2528. doi: 10.3892/mmr.2017.6862

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Copyright: © Jiang et al.

This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Figure 2. — miR-21 promotes neurite outgrowth in rat spinal cord neurons. (A) Neurite outgrowth (detected by β-III tubulin in red) observed in control or miR-21-transfected spinal cord neurons. Scale bar, 100 µm. (B) miR-21 increased the mean length of the longest neurite (per neuron) compared with the control group (n=5/group). (C) Representative western blot images and (D) quantification of PDCD4 protein expression levels following transfection with pri-miR-21 or in-miR-21. β-actin served as an internal control. miR-21 significantly downregulated the expression levels of PDCD4. Data are expressed as the mean ± standard deviation (n=4/group). *P<0.05 vs. control group. miR-21, microRNA-21; PDCD4, programmed cell death 4; PTEN, phosphatase and tensin homolog; pri, primary; in, inhibitor; nc, negative control.