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      MicroRNA Expression in β-Thalassemia and Sickle Cell Disease: A Role in The Induction of Fetal Hemoglobin

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          Abstract

          Today the regulatory role of microRNAs (miRs) is well characterized in many diverse cel- lular processes. MiR-based regulation is categorized under epigenetic regulatory mecha- nisms. These small non-coding RNAs participate in producing and maturing erythrocytes, expressing hematopoietic factors and regulating expression of globin genes by post-tran- scriptional gene silencing. The changes in expression of miRs (miR-144/-320/-451/-503) in thalassemic/sickle cells compared with normal erythrocytes may cause clinical severity. According to the suppressive effects of certain miRs (miR-15a/-16-1/-23a/-26b/-27a/-451) on a number of transcription factors [myeloblastosis oncogene ( MYB), B-cell lymphoma 11A (BCL11A), GATA1, Krüppel-like factor 3 ( KLF3) and specificity protein 1 ( Sp1)] during β globin gene expression, It has been possible to increasing γ globin gene expression and fetal hemoglobin (HbF) production. Therefore, this strategy can be used as a novel therapy in infusing HbF and improving clinical complications of patients with hemoglobi- nopathies.

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          An important role of Nrf2-ARE pathway in the cellular defense mechanism.

          Jong-Min Lee, Jeffrey A Johnson (2004)
          The antioxidant responsive element (ARE) is a cis-acting regulatory element of genes encoding phase II detoxification enzymes and antioxidant proteins, such as NAD(P)H: quinone oxidoreductase 1, glutathione S-transferases, and glutamate-cysteine ligase. Interestingly, it has been reported that Nrf2 (NF-E2-related factor 2) regulates a wide array of ARE-driven genes in various cell types. Nrf2 is a basic leucine zipper transcription factor, which was originally identified as a binding protein of locus control region of beta-globin gene. The DNA binding sequence of Nrf2 and ARE sequence are very similar, and many studies demonstrated that Nrf2 binds to the ARE sites leading to up-regulation of downstream genes. The function of Nrf2 and its downstream target genes suggests that the Nrf2-ARE pathway is important in the cellular antioxidant defense system. In support of this, many studies showed a critical role of Nrf2 in cellular protection and anti-carcinogenicity, implying that the Nrf2-ARE pathway may serve as a therapeutic target for neurodegenerative diseases and cancers, in which oxidative stress is closely implicated.
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            MicroRNAs 221 and 222 inhibit normal erythropoiesis and erythroleukemic cell growth via kit receptor down-modulation.

            Nadia Felli, Laura Fontana, Elvira Pelosi … (2005)
            MicroRNAs (miRs) are small noncoding RNAs that regulate gene expression primarily through translational repression. In erythropoietic (E) culture of cord blood CD34+ progenitor cells, the level of miR 221 and 222 is gradually and sharply down-modulated. Hypothetically, this decline could promote erythropoiesis by unblocking expression of key functional proteins. Indeed, (i) bioinformatic analysis suggested that miR 221 and 222 target the 3' UTR of kit mRNA; (ii) the luciferase assay confirmed that both miRs directly interact with the kit mRNA target site; and (iii) in E culture undergoing exponential cell growth, miR down-modulation is inversely related to increasing kit protein expression, whereas the kit mRNA level is relatively stable. Functional studies show that treatment of CD34+ progenitors with miR 221 and 222, via oligonucleotide transfection or lentiviral vector infection, causes impaired proliferation and accelerated differentiation of E cells, coupled with down-modulation of kit protein: this phenomenon, observed in E culture releasing endogenous kit ligand, is magnified in E culture supplemented with kit ligand. Furthermore, transplantation experiments in NOD-SCID mice reveal that miR 221 and 222 treatment of CD34+ cells impairs their engraftment capacity and stem cell activity. Finally, miR 221 and 222 gene transfer impairs proliferation of the kit+ TF-1 erythroleukemic cell line. Altogether, our studies indicate that the decline of miR 221 and 222 during exponential E growth unblocks kit protein production at mRNA level, thus leading to expansion of early erythroblasts. Furthermore, the results on kit+ erythroleukemic cells suggest a potential role of these miRs in cancer therapy.
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              Rapid destruction of human Cdc25A in response to DNA damage.

              J Bartek, Ronald Lukas, M Welcker … (2000)
              To protect genome integrity and ensure survival, eukaryotic cells exposed to genotoxic stress cease proliferating to provide time for DNA repair. Human cells responded to ultraviolet light or ionizing radiation by rapid, ubiquitin- and proteasome-dependent protein degradation of Cdc25A, a phosphatase that is required for progression from G1 to S phase of the cell cycle. This response involved activated Chk1 protein kinase but not the p53 pathway, and the persisting inhibitory tyrosine phosphorylation of Cdk2 blocked entry into S phase and DNA replication. Overexpression of Cdc25A bypassed this mechanism, leading to enhanced DNA damage and decreased cell survival. These results identify specific degradation of Cdc25A as part of the DNA damage checkpoint mechanism and suggest how Cdc25A overexpression in human cancers might contribute to tumorigenesis.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Cell J
                Journal ID (iso-abbrev): Cell J
                Journal ID (publisher-id): Royan Institute
                Title: Cell Journal (Yakhteh)
                Publisher: Royan Institute
                ISSN (Print): 2228-5806
                ISSN (Electronic): 2228-5814
                Publication date (Print): Winter 2016
                Publication date (Electronic): 17 January 2016
                Volume: 17
                Issue: 4
                Pages: 583-592
                Affiliations
                [1 ]Health Research Institute, Research Center of Thalassemia and Hemoglobinopathy, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
                [2 ]Department of Hematology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran
                [3 ]Department of Medical Genetics, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
                Author notes
                [ *Corresponding Address: ]P.O. Box: 14115-111Department of HematologyFaculty of Medical SciencesTarbiat Modares University TehranIran Email: abroun@ 123456modares.ac.ir
                Article
                Other ID: Cell-J-17-583
                PMC ID: 4746408
                PubMed ID: 26862517
                SO-VID: 37776302-9867-4ade-a058-c16dfc3d5331
                Copyright © Any use, distribution, reproduction or abstract of this publication in any medium, with the exception of commercial purposes, is permitted provided the original work is properly cited
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 27 August 2014
                Date accepted : 11 January 2015
                Categories
                Subject: Review Article
                Subject: Hematology
                Subject: Genetics
                Custom metadata
                Citation Saki N, Abroun S, Soleimani M, Kavianpour M, Shahjahani M, Mohammadi-Asl J, Hajizamani S. MicroRNA expression in β-thalassemia and sickle cell disease: a role in the induction of fetal hemoglobin. Cell J. 2016; 17(4): 583-592.

                Keywords: micrornas,β-thalassemia,sickle cell disease,fetal hemoglobin
                Data availability:
                Keywords: micrornas, β-thalassemia, sickle cell disease, fetal hemoglobin

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