MicroRNA‑21 regulates cell proliferation and apoptosis in H2O2‑stimulated rat spinal cord neurons

Jiao,Genlong; Pan,Bin; Zhou,Zhigang; Zhou,Lin; Li,Zhizhong; Zhang,Ziyong

doi:10.3892/mmr.2015.4265

MicroRNA‑21 regulates cell proliferation and apoptosis in H2O2‑stimulated rat spinal cord neurons

Authors:
- Genlong Jiao
- Bin Pan
- Zhigang Zhou
- Lin Zhou
- Zhizhong Li
- Ziyong Zhang
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Affiliations: Department of Orthopedics, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510632, P.R. China, Department of Surgery, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong 510632, P.R. China, College of Life Science and Technology, Jinan University, Guangzhou, Guangdong 510632, P.R. China
Published online on: August 28, 2015 https://doi.org/10.3892/mmr.2015.4265
Pages: 7011-7016

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Abstract

Oxidative stress can alter the expression level of microRNAs (miRNAs) and has a role in oxidative damage generated by reactive oxygen species (ROS). While previous studies have demonstrated that miR‑146a, miR‑21 and miR‑150 are essential for ROS production in heart disease, the role of these miRNAs in spinal cord injuries has not yet been examined. The present study focused on examining the role of miR‑146a, miR‑21 and miR‑150 during H2O2 stimulation in rat neuronal spinal cord (RN‑sc) cells. RN‑sc cells were treated with H2O2, and cells were harvested for reverse transcription quantitative polymerase chain reaction (RT‑qPCR) to detect the expression levels of miR‑146a, miR‑21 and miR‑150. The results demonstrated that miR‑146a, miR‑21 and miR‑150 expression was upregulated during H2O2 treatment. T-cell death and apoptosis were investigated using an MTT assay and flow cytometric analysis, respectively. Following miR‑21 silencing, H2O2‑induced cell death and apoptosis were reduced in RN‑sc cells, while miR‑150 silencing had no effect. Furthermore, Smad7 was identified as a direct target of miR‑21 using a Luciferase reporter assay, RT-qPCR and western blot analysis. In addition, while H2O2 downregulated Smad7 protein expression, this was reversed by inhibiting miR‑21 expression. Based on previous studies, it was predicted that miR‑21 has a role in ROS production through regulating Smad7 in rat spinal cord neurons.

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