Research Paper Volume 12, Issue 9 pp 7660—7678

Figure 4. miR-221-3p targets NPTX2. The potential target genes of miR-221-3p predicted in the PD-related microarray data GSE20153, which was retrieved from the GEO database. (A) Differential analysis of the differentially expressed genes (DEGs) in normal and PD samples in GSE20153. (B) The expression patterns of the overlapped 8 genes measured by RT-qPCR, *p < 0.05 vs. the cells treated with NC mimic. (C) The expression patterns of NPTX2 in the SNc tissues of PD mouse models measured by Western blot analysis (n = 10), *p < 0.05 vs. mice injected with normal saline. (D) The expression patterns of NPTX2 in PD cell models measured using Western blot analysis, *p < 0.05 vs. the cells treated with PBS. (E) The complementary base paring diagram of miR-221-3p and NPTX2 predicted by an online website. (F) The binding of miR-221-3p to NPTX2 confirmed by dual-luciferase reporter gene assay, *p < 0.05 vs. cells treated with NC mimic. (G) Pearson’s correlation analysis of the expressions of HOTAIR and NPTX2 in the SNc tissues of PD mouse models. (H) The effect of over-expressed or down-regulated HOTAIR on the expression of NPTX2 measured by Western blot analysis, *p < 0.05 vs. cells treated with oe-NC, #p < 0.05 vs. cells treated with sh-NC. (I) Data (mean ± standard deviation) between two groups or among multiple groups were analyzed using unpaired t-test. The experiment was repeated three times. miR-221-3p, microRNA-221-3p; NPTX2, neuronal pentraxin II; GEO, Gene Expression Omnibus; RT-qPCR, reverse transcription quantitative polymerase chain reaction; NC, negative control; SNc, substantia nigra compact; PD, Parkinson’s disease; PBS, phosphate buffered saline; wt, wild type; mut, mutase.