Involvement of miRNA in Erythroid Differentiation

Abstract

miRNAs are a family of small ncRNAs that regulate gene expression by targeting mRNAs in a sequence-specific manner, inducing translational repression or mRNA degradation. In this review, we present and discuss the available literature on the expression of miRNAs in erythroid cells. There are several experimental systems that can be employed for studies focusing on the relationship between miRNAs and erythroid differentiation, including human embryonic stem cells forced to erythroid differentiation, K562 and UT-7 cells induced to hemoglobin production by chemical compounds, erythropoietin-treated erythroid precursor cells from normal subjects or patients affected by hematological disease and in vivo systems, such as zebrafish embryos. Several miRNAs were identified as deeply involved in the erythroid phenotype, including miR-15a, miR-16–1, miR-126, miR-144, miR-451 and miR-210. Several functions related with erythroid cells were demonstrated to be regulated by these miRNAs, including maturation and proliferation of early erythroid cells, expression of fetal γ-globin genes and enucleation. These identified erythroid specific miRNAs represent the starting point to develop new protocols for miRNA therapeutics, based on both anti-miR molecules or miRNA replacement.

KEYWORDS::

• β-thalassemia
• erythroid differentiation
• globin genes
• HbF
• miRNA

Financial & competing interests disclosure

R Gambari is granted by Fondazione Cariparo (Cassa di Risparmio di Padova e Rovigo), CIB, by UE ITHANET Project (eInfrastructure for the Thalassaemia Research Network), by Telethon (contract GGP10214) and by COFIN-2007. This research is also supported by Associazione Veneta per la Lotta alla Talassemia (AVLT), Rovigo. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

R Gambari is granted by Fondazione Cariparo (Cassa di Risparmio di Padova e Rovigo), CIB, by UE ITHANET Project (eInfrastructure for the Thalassaemia Research Network), by Telethon (contract GGP10214) and by COFIN-2007. This research is also supported by Associazione Veneta per la Lotta alla Talassemia (AVLT), Rovigo. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript.