Abstract

Objectives: To explore the mechanism of has-miR-22-3p in H type essential hypertension patients, and to identify the related bioinformatics analysis. Methods: 50 H type essential hypertension patients (H group), 50 essential hypertension patients without homocysteine (Hcy) increased (EH group), and 50 non- EH patients (Control group) were enrolled, plasma Hcy levels were tested by ELISA, and plasma has-miR-22-3p were analyzed by qRT-PCR, and its target genes, biological information, GO function, KEGG pathway, related lncRNAs and circRNA were predicted; using 3’-UTR luciferase reporter assay to determine whether has-miR-22-3p directly binds to the MTHFR -3’UTR. Results: Plasma Hcy levels in H group (13.95 ± 0.72 μmol/L, N = 50) were higher than EH group (9.78 ± 0.85 μmol/L, N = 50) and Control group (9.66 ± 0.98 μmol/L, N = 50) (P < 0.05); bioinformatics analysis found that MTHFR was regulated by has-miR-22-3p, and may participate in Formyltetrahydroformate biosynthesis, etc; hsa-miR-22-3p may be interact with some lncRNAs and circRNAs; 3’-UTR luciferase reporter assay found that has-miR-22-3p directly binds to the MTHFR -3’UTR. H group patients plasma has-miR-22-3p (0.26 ± 0.03, N = 50) were increased higher than EH group (0.04 ± 0.01, N = 50) and Control group (0.03 ± 0.01, N = 50) (P < 0.05); has-miR-22-3p and Hcy Pearson correlation coefficient was 0.59 (P = 0.0079). ROC curve analysis of Hcy found that the area under curve is 0.76 (P < 0.0001), and has-miR-22-3p's area under curve is 0.88 (P < 0.0001). Conclusion: Hcy and has-miR-22-3p can be a novel biomarker of H type essential hypertension, and has-miR-22-3p may participate in the mechanism of H type essential hypertension by regulating MTHFR activity, then reduced the high Hcy, resulting in the occurrence of cardiovascular disease; and may be associated with some lncRNA and circRNA.

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