Downregulation of CCL2 induced by the upregulation of microRNA-206 is associated with the severity of HEV71 encephalitis
Affiliations: Department of Pediatrics, Taian Central Hospital, Taian, Shandong 271000, P.R. China, Department of Pediatrics, Qilu Hospital of Shandong University, Jinan, Shandong 250012, P.R. China
- Published online on: August 2, 2017 https://doi.org/10.3892/mmr.2017.7142
- Pages: 4620-4626
Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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MicroRNAs (miRNAs) have been investigated widely as key regulators of gene expression in different diseases by affecting the miRNA‑mediated regulatory function. Human enterovirus 71 (HEV71) can cause a series of human diseases, including encephalitis. Chemokine (C‑C motif) ligand 2 (CCL2) is one of the important genes involved in regulating inflammation. However, the mechanisms underlying HEV71 encephalitis mediated by CCL2 remain to be elucidated. In the present study, reverse transcription‑quantitative polymerase chain reaction analysis was used to determine the expression level of miR‑206 and the mRNA expression of CCL2 in samples. Western blot analysis was used to detect the protein levels of CCL2. A luciferase assay was used to verify the miR‑206 target site in CCL2. A CCK‑8 assay and flow cytometry were used to determine cell proliferation and apoptosis. The results demonstrated that miR‑206 was downregulated in severe HEV71 encephalitis. Using bioinformatics analysis, miR‑206 was predicted to target the human CCL2 3'‑untranslated region (3'‑UTR). A dual‑luciferase assay demonstrated that miR‑206 downregulated the expression of CCL2 by directly targeting its 3'‑UTR, whereas CCL2 3'‑UTR mutations completely eliminated its interaction with miR‑206. The expression levels of miR‑206 and CCL2 were inversely correlated in cerebrospinal fluid. The expression of exogenous miRNA, which mimicked miR‑206 miRNA, decreased the protein and mRNA levels of CCL2, whereas the suppression of endogenous miR‑206 resulted in an increase of the protein and mRNA levels of CCL2. The present study also found that miR‑206 promoted NPC cell proliferation and reduced the apoptosis of NPC cells via CCL2. The mechanism is likely to involve suppression of the expression of miR‑206 and upregulation of the expression of CCL2, important in regulating the progress of HEV71 encephalitis. In conclusion, miR‑206 may be useful in the prognosis and treatment of HEV71 encephalitis.