ArticleMolecular medicine reports2017
Downregulation of CCL2 induced by the upregulation of microRNA-206 is associated with the severity of HEV71 encephalitis.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.
- Pooled it
- Regulatory role of microRNAs in virus-mediated inflammation.Journal of inflammation (London, England) · 2024Review
- Roles of Non-Coding RNAs in Virus-Host Interaction About Pathogenesis of Hand-Foot-Mouth Disease.Current microbiology · 2022Review
- Loss of RNA binding protein HuD facilitates the production of the senescence-associated secretory phenotype.Cell death & disease · 2022Article
- Transcriptome of human neuroblastoma SH-SY5Y cells in response to 2B protein of enterovirus-A71.Scientific reports · 2022Article
- DNA methylation and gene expression profiles to identify childhood atopic asthma associated genes.BMC pulmonary medicine · 2021Article
- High Expression MicroRNA-206 Inhibits the Growth of Tumor Cells in Human Malignant Fibrous Histiocytoma.Frontiers in cell and developmental biology · 2021Article
- Innate Immune Functions of Astrocytes are Dependent Upon Tumor Necrosis Factor-Alpha.Scientific reports · 2020Article
- Acute 4,4'-Methylene Diphenyl Diisocyanate Exposure-Mediated Downregulation of miR-206-3p and miR-381-3p Activates Inducible Nitric Oxide Synthase Transcription by Targeting Calcineurin/NFAT Signaling in Macrophages.Toxicological sciences : an official journal of the Society of Toxicology · 2020Article
- Picornaviruses and RNA Metabolism: Local and Global Effects of Infection.Journal of virology · 2019Review
- miR-146a deficiency does not aggravate muscular dystrophy in mdx mice.Skeletal muscle · 2019Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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