miR-26a prevents neural stem cells from apoptosis via β-catenin signaling pathway in cardiac arrest-induced brain damage

Abstract

Neural stem cells (NSCs) transplantation is one of the most promising strategies for the treatment of CA-induced brain damage. The transplanted NSCs could differentiate into new neuron and replace the damaged one. However, the poor survival of NSCs in severe hypoxic condition is the limiting step to make the best use of this kind of therapy. In the present study, we investigated whether the overexpression of miR-26a improves the survival of NSCs in hypoxic environment in vitro and in vivo. In vitro hypoxia injury model is established in NSCs by CoCl2 treatment, and in vivo cardiac arrest (CA) model is established in Sprague-Dawley (SD) rats. Quantitative real-time polymerase chain reaction is used to detect the mRNA level and Western blot is used to examine the protein level of indicated genes. TUNEL staining and flow cytometry are applied to evaluate apoptosis. Dual-luciferase reporter assay is utilized to analyze the target gene of miR-26a. The expression of miR-26a is reduced in both in vitro and in vivo hypoxic model. MiR-26a directly targets 3′-UTR of glycogen synthase kinase 3β (GSK-3β), resulting in increased β-catenin expression and decreased apoptosis of NSCs. Overexpression of miR-26a in transplanted NSCs improves the survival of NSCs and neurological function in CA rats. MiR-26a prevents NSCs from apoptosis by activating β-catenin signaling pathway in CA-induced brain damage model. Modulating miR-26a expression could be a potential strategy to attenuate brain damage induced by CA.

Resetting Proteostasis of CIRBP with ISRIB Suppresses Neural Stem Cell Apoptosis under Hypoxic Exposure

“…Oxygen concentration may occur to be below 1% in the onset area of pathological hypoxic diseases, such as acute plateau edema, stroke and cerebral embolism, and brain tumors, and in even severe cases [52,53], anoxia may happen. According to early studies, 1% oxygen concentration significantly impeded the speed of proliferation and reduced the amount of NSCs [18], and the prolonged excessive hypoxia caused a considerable rise in NSC apoptosis and therefore could lead to irreversible damage to the nervous system [54,55]. Our studies revealed that prolonged hypoxic exposure could significantly induce apoptosis of NSCs and decrease the number of those cells.…”

The protective effects of microRNA-26a in steroid-induced osteonecrosis of the femoral head by repressing EZH2

“…cardiac arrest-induced brain damage by the activation of the β-catenin signaling pathway [32]. Moreover, we have found that the elevated miR-26a and restrained EZH2 could ameliorate the apoptosis of osteoblasts in SONFH by repressing Bax and elevating Bcl-2.…”

MicroRNA-26a-3p rescues depression-like behaviors in male rats via preventing hippocampal neuronal anomalies

“…MiR-26a, a brain-enriched microRNA mainly localized within axonal compartments of neurons, has been hypothesized to play a key role in axon development and regeneration (41,42), and also involved in the formation, maturation and/or plasticity of synapses via regulating distinct sets of target genes (43). For example, it has been suggested that miR-26a is involved in regulating excitatory neurotransmission under stress condition (44), and maintains stress resiliency and antidepressant efficacy by targeting the serotonergic autoreceptor (33).…”