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Please use this identifier to cite or link to this item: http://repository.li.mahidol.ac.th/dspace/handle/123456789/41141
Title: Elevated levels of miR-210 correlate with anemia in β-thalassemia/HbE patients
Authors: Panjaree Siwaponanan
Suthat Fucharoen
Pornpan Sirankapracha
Pranee Winichagoon
Tsukuru Umemura
Saovaros Svasti
Mahidol University
Kyushu University
International University of Health and Welfare
Keywords: Medicine
Issue Date: 1-Sep-2016
Citation: International Journal of Hematology. Vol.104, No.3 (2016), 338-343
Abstract: © 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.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84983631364&origin=inward
http://repository.li.mahidol.ac.th/dspace/handle/123456789/41141
ISSN: 18653774
09255710
Appears in Collections:Scopus 2016-2017

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