Microrna Expression in Β-Thalassemia and Sickle Cell Disease: A Role in the Induction of Fetal Hemoglobin

Today the regulatory role of micrornas (mirs) is well characterized in many diverse cellular processes. mir-based regulation is categorized under epigenetic regulatory mechanisms. these small non-coding rnas participate in producing and maturing erythrocytes, expressing hematopoietic factors and regulating expression of globin genes by post-transcriptional gene silencing. the changes in expression of mirs (mir-144/-320/-451/-503) in thalassemic/sickle cells compared with normal erythrocytes may cause clinical severity. according to the suppressive effects of certain mirs (mir-15a/-16-1/-23a/-26b/-27a/-451) on a number of transcription factors [myeloblastosis oncogene (myb), b-cell lymphoma 11a (bcl11a), gata1, krüppel-like factor 3 (klf3) and specificity protein 1 (sp1)] during β globin gene expression, it has been possible to increasing γ globin gene expression and fetal hemoglobin (hbf) production. therefore, this strategy can be used as a novel therapy in infusing hbf and improving clinical complications of patients with hemoglobinopathies.