MiR-29b Modulates Bone Marrow Mesenchymal Stem Cells (BMSCs) Differentiation and Induces Nerve Repair in Diabetic Retina Rat Model

Abstract

microRNAs are involved in diabetic retinopathy (DR). This study intends to analyze miR-29b’s role in bone marrow mesenchymal stem cells (BMSCs) differentiation in DR rat models to induce nerve repair. BMSCs from DR rat models were cultured and transfected with miR-29b mimics and inhibitors followed by measuring miR-29b level, cell proliferation and apoptosis. Retinal ganglion cells (RGC) were treated with high glucose for 24 h, and BMSCs and si-miR-29b-BMSC were cocultured for 24 h, respectively followed by assessing cell proliferation and apoptosis, inflammatory cytokines by ELISA, MDA, SOD, brain-derived neurotrophic factor (BDNF) and ciliary neurotrophic factor (CNTF) level by ELISA. MiR-29b was up-regulated in BMSCs of DR rats. miR-29b mimics significantly up-regulated miR-29b, inhibited cell proliferation and promoted apoptosis (P < 0.05), which were reversed by miR-29b inhibitor (P < 0.05). Co-culture of BMSCs with si-miR-29b-BMSC promoted RGC proliferation, inhibited apoptosis and IL-6 secretion, decreased MDA, increased SOD, BDNF and CNTF expression (P < 0.05) with more significant changes in si-miR-29b-BMSC group (P < 0.05). In conclusion, down-regulation of miR-29b promotes BMSCs proliferation in DR rat models, inhibits BMSCs apoptosis, and promotes the recovery of retinal ganglion cell function.