Article

MicroRNAs: Allies or foes in erythropoiesis?

Division of Hematology, Department of Medicine, University of Washington, Seattle, Washington, USA.
Journal of Cellular Physiology (impact factor: 3.87). 03/2011; 227(1):7-13. DOI:10.1002/jcp.22729 pp.7-13
Source: PubMed

ABSTRACT MicroRNAs are small non-coding RNAs that negatively regulate gene expression through mRNA degradation or translational repression. It is becoming increasingly recognized that miRNAs play central roles in almost all cellular processes, and especially during development. The function of miRNAs in hematopoiesis, including erythropoiesis, is beginning to be elucidated. In this review, we will focus on what is known about miRNA function in various aspects of erythropoiesis and red cell physiology.

0 0
 · 
0 Bookmarks
 · 
43 Views
  • Source
    Article: MicroRNA-486-3p Regulates γ-Globin Expression in Human Erythroid Cells by Directly Modulating BCL11A.
    Valentina Lulli, Paolo Romania, Ornella Morsilli, Paolo Cianciulli, Marco Gabbianelli, Ugo Testa, Alessandro Giuliani, Giovanna Marziali
    [show abstract] [hide abstract]
    ABSTRACT: MicroRNAs (miRNAs) play key roles in modulating a variety of cellular processes through repression of mRNAs target. The functional relevance of microRNAs has been proven in normal and malignant hematopoiesis. While analyzing miRNAs expression profile in unilineage serum-free liquid suspension unilineage cultures of peripheral blood CD34(+) hematopoietic progenitor cells (HPCs) through the erythroid, megakaryocytic, granulocytic and monocytic pathways, we identified miR-486-3p as mainly expressed within the erythroid lineage. We showed that miR-486-3p regulates BCL11A expression by binding to the extra-long isoform of BCL11A 3'UTR. Overexpression of miR-486-3p in erythroid cells resulted in reduced BCL11A protein levels, associated to increased expression of γ-globin gene, whereas inhibition of physiological miR-486-3p levels increased BCL11A and, consequently, reduced γ-globin expression. Thus, miR-486-3p regulating BCL11A expression might contributes to fetal hemoglobin (HbF) modulation and arise the question as to what extent this miRNA might contribute to different HbF levels observed among β-thalassemia patients. Erythroid cells, differentiated from PB CD34(+) cells of a small cohort of patients affected by major or intermedia β-thalassemia, showed miR-486-3p levels significantly higher than those observed in normal counterpart. Importantly, in these patients, miR-486-3p expression correlates with increased HbF synthesis. Thus, our data indicate that miR-486-3p might contribute to different HbF levels observed among thalassemic patients and, possibly, to the clinical severity of the disease.
    PLoS ONE 01/2013; 8(4):e60436. · 4.09 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.

Keywords

cellular processes
 
central roles
 
erythropoiesis
 
miRNA function
 
miRNAs
 
mRNA degradation
 
negatively regulate gene expression
 
red cell physiology
 
various aspects