Elevated levels of miR-210 correlate with anemia in [beta]-thalassemia/HbE patients

• Published in: International journal of hematology 2016-09, Vol.104 (3), p.338
• Main Authors: Siwaponanan, Panjaree, Fucharoen, Suthat, Sirankapracha, Pornpan, Winichagoon, Pranee, Umemura, Tsukuru, Svasti, Saovaros
• Format: Article
• Language: English
• ISSN: 0925-5710; 1865-3774
• DOI: 10.1007/s12185-016-2032-0

Ineffective erythropoiesis in [beta]-thalassemia patients is caused by the premature death of red blood cell precursors due to excess [alpha]-globin chains. As a consequence, patients develop chronic anemia and hypoxia. Upregulation of miR-210, a hypoxia-induced miRNA, has been shown to regulate globin gene expression and erythroid differentiation in [beta]-thalassemia/HbE erythroid progenitor cell culture. The present study examined whether the expression of miR-210 in circulation reflects the anemic condition in these patients. The level of miR-210 expression was directly examined from red blood cells and plasma of [beta]-thalassemia/HbE patients. Transferrin receptor, a marker of erythropoiesis activity, was also analyzed. Increased expression of both red blood cells and plasma miR-210 as well as elevated levels of serum transferrin receptor in [beta]-thalassemia/HbE patients were observed when compared to those of normal individuals (p < 0.05). In addition, red blood cell miR-210 level was inversely correlated with hemoglobin levels (r = -0.7054, p < 0.01) and hematocrit (r = -0.6017, p < 0.05). The higher expression of miR-210 in these patients may be the consequence of hypoxia occurring from the lower hemoglobin level. Thus, analysis of red blood cell miR-210 may be useful as a method for assessing hypoxia in [beta]-thalassemia patients.