Panjaree SiwaponananSuthat FucharoenPornpan SirankaprachaPranee WinichagoonTsukuru UmemuraSaovaros SvastiMahidol UniversityKyushu UniversityInternational University of Health and Welfare2018-12-112019-03-142018-12-112019-03-142016-09-01International Journal of Hematology. Vol.104, No.3 (2016), 338-34318653774092557102-s2.0-84983631364https://repository.li.mahidol.ac.th/handle/20.500.14594/41141© 2016, The Japanese Society of Hematology. Ineffective erythropoiesis in β-thalassemia patients is caused by the premature death of red blood cell precursors due to excess α-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 β-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 β-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 β-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 β-thalassemia patients.Mahidol UniversityMedicineArticleSCOPUS10.1007/s12185-016-2032-0