Journal
MOLECULAR BIOLOGY REPORTS
Volume 47, Issue 5, Pages 3909-3918Publisher
SPRINGER
DOI: 10.1007/s11033-020-05483-7
Keywords
beta-thalassemia; miR-30a; HbF; BCL11A
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Patients with beta-thalassemia suffer from a lack or absence of the beta-globin chain of normal hemoglobin (Hb). Therefore, an increase in fetal Hb (HbF) levels could improve the clinical status of these patients. Downregulation of BCL11A, a key regulatory transcription factor, could ameliorate the clinical status of thalassemic patients by increasing HbF levels. miR-30a expression and its relationship with the BCL11A gene in erythroid precursors was explored in patients with beta-thalassemia. The relevance of miR-30a to clinical parameters was also investigated. We evaluated the expressions of miR-30a, BCL11A, and gamma-globin genes by quantitative real-time PCR (qRT-PCR) on isolated erythroid precursors from peripheral blood samples of beta-thalassemia intermedia (TI) patients and in bone marrow samples from healthy individuals as controls. The correlation between miR-30a expression and clinical indices that included HbF levels, ferritin, and the frequency of blood transfusions were assessed. We observed increased expression of miR-30a in conjunction with decreased BCL11A expression and elevated gamma-globin and HbF levels. Patients with elevated miR-30a expression had a higher percentage of HbF and a lower level of ferritin. In addition, we observed that overexpression of miR-30a in erythroid precursor cells led to reduced BCL11A expression and was associated with elevated gamma-globin expression. Our findings showed the importance of miR-30a in BCL11A and HbF regulation, and in the clinical status of patients with beta-thalassemia
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