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Enhanced erythroid cell differentiation in hypoxic condition is in part contributed by miR-210.

Abstract
Erythropoiesis, a process of erythroid production, is controlled by several factors including oxygen level. In this study, the effect of oxygen tension on erythropoiesis was investigated in K562 erythroleukemic cell line and erythroid progenitor cells derived from normal and β-thalassemia/hemoglobin (Hb) E individuals. The enhanced erythroid differentiation specific markers including increased levels of α-, β- and γ-globin gene expressions, numbers of HbF positive cells and the presence of glycophorin A surface marker were observed during cell culture under hypoxic atmosphere. The result also showed that miR-210, one of the hypoxia-induced miRNAs, was up-regulated in K562 and β-thalassemia/HbE progenitor cells cultured under hypoxic condition. Inhibition of miR-210 expression leads to reduction of the globin gene expression and delayed maturation in K562 and erythroid progenitor cells. This indicated that miR-210 contributes to hypoxia-induced erythroid differentiation in both K562 cells and β-thalassemia/HbE erythroid progenitor cells.
AuthorsOrawan Sarakul, Phantip Vattanaviboon, Yuka Tanaka, Suthat Fucharoen, Yasunobu Abe, Saovaros Svasti, Tsukuru Umemura
JournalBlood cells, molecules & diseases (Blood Cells Mol Dis) Vol. 51 Issue 2 Pg. 98-103 (Aug 2013) ISSN: 1096-0961 [Electronic] United States
PMID23623309 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright © 2013 Elsevier Inc. All rights reserved.
Chemical References
  • Antigens, CD34
  • MIRN210 microRNA, human
  • MicroRNAs
  • RNA, Messenger
  • Globins
Topics
  • Antigens, CD34 (metabolism)
  • Cell Differentiation
  • Cell Hypoxia
  • Erythroid Cells (cytology, metabolism)
  • Erythroid Precursor Cells (cytology, metabolism)
  • Erythropoiesis (genetics)
  • Gene Expression Regulation
  • Globins (genetics, metabolism)
  • Humans
  • Immunophenotyping
  • K562 Cells
  • MicroRNAs (genetics)
  • RNA, Messenger (genetics, metabolism)
  • beta-Thalassemia (genetics, metabolism)

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