SNHG12 inhibits oxygen‑glucose deprivation‑induced neuronal apoptosis via the miR‑181a‑5p/NEGR1 axis
- Yangtian Yan
- Li Chen
- Jiajun Zhou
- Liquan Xie
Affiliations: Department of Neurology, Wenling Hospital of Traditional Chinese Medicine, Wenling, Zhejiang 317500, P.R. China, Department of Neurosurgery, the Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310005, P.R. China, Department of Neurology, Xixi Hospital of Hangzhou, Hangzhou, Zhejiang 310023, P.R. China, Department of Gerontology, Hangzhou Hospital of Traditional Chinese Medicine, Hangzhou, Zhejiang 310007, P.R. China
- Published online on: August 24, 2020 https://doi.org/10.3892/mmr.2020.11459
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Emerging evidence has indicated that long non‑coding RNAs (lncRNAs) are closely associated with the pathogenesis of ischemic stroke. It has been reported that small nucleolar RNA host gene 12 (SNHG12) serves a critical role in ischemic stroke by acting as a competitive endogenous RNA (ceRNA). SNHG12 competes with various microRNAs (miRs) to regulate RNA transcription of specific targets. However, the effect of SNHG12 on oxygen‑glucose deprivation (OGD)‑induced neuronal apoptosis has rarely been reported. The present study demonstrated that SNHG12 expression was downregulated in OGD‑injured SH‑SY5Y cells. Furthermore, miR‑181a‑5p was reported as a target of SNHG12 and was negatively regulated by SNHG12. Moreover, NEGR1 was a target of miR‑181a‑5p, which functions as a negative regulator of NEGR1 in OGD‑induced neuronal apoptosis. In summary, the results strongly confirmed the hypothesis that SNHG12 functions as a ceRNA for miR‑181a‑5p and regulates the expression of NEGR1 thus inhibiting OGD‑induced apoptosis of SH‑SY5Y cells. Neuronal apoptosis aggravates brain damage during ischemic stroke, indicating that the activation of SNHG12 and NEGR1 expression and inhibition of miR‑181a‑5p may be a novel strategy for the clinical treatment of ischemic stroke.