Abstract：
:Patients with β-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 β-thalassemia. The relevance of miR-30a to clinical parameters was also investigated. We evaluated the expressions of miR-30a, BCL11A, and γ-globin genes by quantitative real-time PCR (qRT-PCR) on isolated erythroid precursors from peripheral blood samples of β-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 γ-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 γ-globin expression. Our findings showed the importance of miR-30a in BCL11A and HbF regulation, and in the clinical status of patients with β-thalassemia.
journal_name
Mol Biol Repjournal_title
Molecular biology reportsauthors
Gholampour MA,Asadi M,Naderi M,Azarkeivan A,Soleimani M,Atashi Adoi
10.1007/s11033-020-05483-7subject
Has Abstractpub_date
2020-05-01 00:00:00pages
3909-3918issue
5eissn
0301-4851issn
1573-4978pii
10.1007/s11033-020-05483-7journal_volume
47pub_type
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