Journal
INTERNATIONAL JOURNAL OF HEMATOLOGY
Volume 104, Issue 3, Pages 338-343Publisher
SPRINGER JAPAN KK
DOI: 10.1007/s12185-016-2032-0
Keywords
miR-210; Thalassemia; Hypoxia; Hemoglobin
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Funding
- Mahidol University Research Grants
- Office of the Higher Education Commission
- Mahidol University under the National Research University Initiative
- Thailand Research Fund [RMU5380001, IRG5780009]
- Research Chair Grant
- National Science and Technology Development Agency (NSTDA), Thailand
- Japan Society for the Promotion of Science (JSPS) [21659240]
- RGJ scholarship from the Thailand Research Fund
- Grants-in-Aid for Scientific Research [21659240] Funding Source: KAKEN
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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.
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