MicroRNA‑29a promotes the neural differentiation of rat neural stem/progenitor cells by targeting KLF4
- Yunan Gao
- Hu Qiao
- Tianyu Zhong
- Zhen Lu
- Yuxia Hou
Affiliations: Key Laboratory of Shaanxi Province for Craniofacial Precision Medicine Research, College of Stomatology, Xi'an Jiaotong University, Xi'an, Shaanxi 710004, P.R. China, Department of Orthodontics, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China
- Published online on: May 22, 2020 https://doi.org/10.3892/mmr.2020.11177
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Neural stem/progenitor cells (NSPCs) remain in the mammalian brain throughout life, where they have the ability to self‑renew and generate different types of cell in the central nervous system (CNS). Therefore, NSPCs may be a potential novel therapeutic strategy following damage to the CNS. Previous research has reported that microRNA (miR)‑29a served an important role in regulating cell proliferation, differentiation and survival; however, to the best of our knowledge, little is known of the effect of miR‑29a in neural differentiation. The present study aimed to investigate the effect of miR‑29a on the differentiation of NSPCs, determined via RNA interference, immunostaining, reverse transcription-quantitative PCR and western blotting. The present study discovered that the expression levels of miR‑29a were significantly upregulated in a time‑dependent manner during neural differentiation. Immunostaining showed that overexpression of miR‑29a promoted neural differentiation, which manifested in increased expression levels of neuron‑specific class III β‑tubulin (Tuj1); however, miR‑29a had no effect on neuroglial differentiation. The expression levels of Kruppel‑like factor 4 (KLF4) were downregulated following overexpression of miR‑29a, whereas the inhibition of miR‑29a demonstrated the opposite effect. These results suggested that the overexpression of miR‑29a may promote neural differentiation in cultured rat NSPCs by decreasing the expression levels of KLF4. Thus indicating that targeting KLF4, a crucial regulatory factor for the maintenance of stemness, may be a potential underlying mechanism of action for miR‑29a. In conclusion, the findings of the present study identified a potential mechanism of action for miR‑29a in NSPC differentiation and provided a novel insight into the treatment strategies for CNS damage.