Fig. 8

miR-326 promotes autophagy via the PTBP1/PI3K signaling pathway. A The potential binding sites for miR-326 on the 3′UTR of PTBP1. B 293T cells were co-transfected with miR-326 mimic or miRNA control and with a luciferase reporter vector containing WT or mutant 3′UTR of PTBP1. C The expression level of PTBP1 negatively correlated with the level of miR-326 in OM-MSCs. D Compared with those in Hemin-exposed normoxia OM-MSCs, the expression levels of p-PI3K/PI3K and PTBP1 were robustly decreased in Hemin-exposed hypoxia OM-MSCs. E Overexpressed PTBP1 increased the expression of PTBP1 and p-PI3K/PI3K. F Under miR-326 mimics treatment, overexpressed PTBP1 increased the expression of p21, P53, p16INK4A, and P62 protein and decreased the expression of LC3II/I and Bcelin-1 protein. G Treatment with PI3K activator partially reversed the downregulation of p-PI3K/PI3K and P63 and the upregulation of LC3II/I and Bcelin-1 induced by the miR-326 mimics. Data are expressed as the mean ± SEM (n = 3) (^*P <0.05, ^**P <0.01, ^***P <0.001, ns. no significance)