Stem cells from human exfoliated deciduous teeth transmit microRNA-26a to protect rats with experimental intracerebral hemorrhage from cerebral injury via suppressing CTGF

Abstract Objective A large number of studies have shown that stem cells from human exfoliated deciduous teeth (SHED) has a protective effect on brain damage, but its specific mechanism is unclear. This research focused on the effect of microRNA (miR)-26a that transmitted by SHED in intracerebral hemorrhage (ICH). Methods SHED were extracted from deciduous teeth of healthy children and miR-26a expression in SHED was altered through transfection, and then the SHED were conducted with neuron differentiated induction, expression of β3 tubulin, MAP-2 and glial fibrillary acidic protein (GFAP), number of dendritic spines and cell proliferation were detected. ICH rat models were established by stereotactic injection of collagenase VII into the left striatum and the modeled rats were injected with miR-26a mimic/inhibitor-transfected SHED suspension. Then, the brain water content, blood-brain barrier permeability, pathological changes, and injury and apoptosis in the nervous cells in brain were assessed. The expression of miR-26a and CTGF in SHED and rats’ brain tissues was evaluated and the target relation between miR-26a and CTGF was detected. Results In SHED after induction, upregulated miR-26a could increase number of dendritic spines, cell proliferation, and expression of miR-26a, β3 tubulin, MAP-2 and GFAP, and restrain CTGF expression. In rat models, up-regulation of miR-26a could attenuate brain water content, Evans blue content, apoptosis, pathological injury and expression of CTGF and Bax, while promoted number of Nissl bodies and expression of miR-26a and Bcl-2 in the nervous cells in brain in ICH rats. Oppositely, miR-26a down-regulation had totally contrary effects on SHED and ICH rats. Furthermore, miR-26a competitively bound to CTGF. Conclusion Our findings provided the evidence that SHED could transmit miR-26a to protect ICH rats from cerebral injury by repressing CTGF, which may contribute to ICH therapy.