Publication | Open Access
Serum miR‐146a, miR‐155, and miR‐210 as potential markers of Graves’ disease
31
Citations
24
References
2017
Year
ImmunodeficienciesImmunologyImmune RegulationPathologyGraves ’ DiseaseSerum Mir‐146aImmune SystemImmune DysregulationMi Rna SPotential MarkersMolecular DiagnosticsRoc Curve AnalysisSerum LevelsAutoimmune DiseaseAutoimmunityImmune FunctionGene ExpressionEpigenetic RegulationMicrorna DetectionPrognostic BiomarkersImmune Cell DevelopmentNatural SciencesBiomarkersMedicineNon-coding Rna
Background Previous studies have demonstrated that dysfunctional regulatory T cells (Tregs) may be associated with Graves’ disease ( GD ). In this study, we evaluated four serum Treg‐associated mi RNA s (miR‐210, miR‐182, miR‐155, and miR‐146a) expressions and assessed the potential of serum mi RNA s as biomarkers of GD . Methods Foxp3 and serum mi RNA s expressions both in GD patients and healthy controls were measured by RT ‐ PCR . Results Serum miR‐210 in GD patients was significantly higher than that of healthy controls (2.64‐fold, P <.001); in contrast, miR‐155 and miR‐146a were lower ( P <.001 and P =.008). No significant difference was found in miR‐182. ROC curve analysis indicated that miR‐210, miR‐155, and miR‐146a with the area under ROC ( AUC ) of 0.803 (70.0% sensitivity and 83.1% specificity), 0.796 (76.3% sensitivity and 76.9% specificity), and 0.736 (68.8% sensitivity and 73.8% specificity), respectively, could differentiate GD patients from healthy controls. Combination of three mi RNA s yielded an AUC of 0.976 (91.3% sensitivity and 93.8% specificity) with 92.41% diagnostic efficiency. In addition, serum miR‐210 and miR‐155 in GD were associated with the extent of goiter. Three mi RNA s levels were different by gender. Besides, serum miR‐210 was positively correlated with free thyroxine ( FT 4) and thyrotrophin receptor antibody ( TRA b) level. Conclusion The serum levels of miR‐210, miR‐155, and miR‐146a may be potential new markers for the diagnosis of GD and play important roles in GD pathogenesis.
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