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 Blood, 15 January 2008, Vol. 111, No. 2, pp. 588-595.
Prepublished online as a Blood First Edition Paper on September 28, 2007; DOI 10.1182/blood-2007-05-092718.

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HEMATOPOIESIS

MicroRNA miR-24 inhibits erythropoiesis by targeting activin type I receptor ALK4

Qiang Wang1, Zheng Huang2, Huiling Xue2, Chengcheng Jin1, Xiu-Li Ju3, Jing-Dong J. Han2, and Ye-Guang Chen1

1 State Key Laboratory of Biomembrane and Membrane Biotechnology, Department of Biological Sciences and Biotechnology, Tsinghua University, Beijing; 2 CAS Key Laboratory of Molecular Developmental Biology and Center for Molecular Systems Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing; and 3 Department of Pediatrics, Qilu Hospital of Shandong University, Jinan, China

MicroRNAs have been suggested to modulate a variety of cellular events. Here we report that miR-24 regulates erythroid differentiation by influencing the expression of human activin type I receptor ALK4 (hALK4). Ectopic expression of miR-24 reduces the mRNA and protein levels of hALK4 by targeting the 3'-untranslated region of hALK4 mRNA and interferes with activin-induced Smad2 phosphorylation and reporter expression. Furthermore, miR-24 represses the activin-mediated accumulation of hemoglobin, an erythroid differentiation marker, in erythroleukemic K562 cells and decreases erythroid colony-forming and burst-forming units of CD34+ hematopoietic progenitor cells. ALK4 expression is inversely correlated with miR-24 expression during the early stages of erythroid differentiation, and the forced expression of miR-24 leads to a delay of activin-induced maturation of hematopoietic progenitor cells in liquid culture. Thus, our findings define a regulation mode of miR-24 on erythropoiesis by impeding ALK4 expression.


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