Up-regulation of microRNA 101-3p during erythropoiesis in β-thalassemia/HbE

Phannasil, Phatchariya; Sukhuma, Chanyanat; Nauphar, Donny; Nuamsee, Khanita; Svasti, Saovaros

doi:10.1016/j.bcmd.2023.102781

Blood Cells, Molecules, and Diseases

2023

DOI: 10.1016/j.bcmd.2023.102781

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Up-regulation of microRNA 101-3p during erythropoiesis in β-thalassemia/HbE

Phatchariya Phannasil,

Chanyanat Sukhuma,

Donny Nauphar

et al.

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2024

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Cited by 4 publications

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Clinical implications of miRNAs in erythropoiesis, anemia, and other hematological disorders

Pal,

Sur,

Mittal

et al. 2024

Mol Biol Rep

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Clinical implications of miRNAs in erythropoiesis, anemia, and other hematological disorders

Pal,

Sur,

Mittal

et al. 2024

Mol Biol Rep

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A Review of Key Regulators of Steady-State and Ineffective Erythropoiesis

Țichil,

Mitre,

Zdrenghea

et al. 2024

JCM

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Erythropoiesis is initiated with the transformation of multipotent hematopoietic stem cells into committed erythroid progenitor cells in the erythroblastic islands of the bone marrow in adults. These cells undergo several stages of differentiation, including erythroblast formation, normoblast formation, and finally, the expulsion of the nucleus to form mature red blood cells. The erythropoietin (EPO) pathway, which is activated by hypoxia, induces stimulation of the erythroid progenitor cells and the promotion of their proliferation and survival as well as maturation and hemoglobin synthesis. The regulation of erythropoiesis is a complex and dynamic interaction of a myriad of factors, such as transcription factors (GATA-1, STAT5), cytokines (IL-3, IL-6, IL-11), iron metabolism and cell cycle regulators. Multiple microRNAs are involved in erythropoiesis, mediating cell growth and development, regulating oxidative stress, erythrocyte maturation and differentiation, hemoglobin synthesis, transferrin function and iron homeostasis. This review aims to explore the physiology of steady-state erythropoiesis and to outline key mechanisms involved in ineffective erythropoiesis linked to anemia, chronic inflammation, stress, and hematological malignancies. Studying aberrations in erythropoiesis in various diseases allows a more in-depth understanding of the heterogeneity within erythroid populations and the development of gene therapies to treat hematological disorders.

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Upregulation of miR‑6747‑3p affects red blood cell lineage development and induces fetal hemoglobin expression by targeting BCL11A in β‑thalassemia

Lv,

Chen,

Zhang

et al. 2024

Mol Med Rep

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in β-thalassemia, excessive α-globin chain impedes the normal development of red blood cells resulting in anemia. numerous mirnas, including mir-6747-3p, are aberrantly expressed in β-thalassemia major (β-TM), but there are no reports on the mechanism of mir-6747-3p in regulating red blood cell lineage development and fetal hemoglobin (HbF) expression. in the present study, rT-qPcr was utilized to confirm miR-6747-3p expression in patients with β-TM and the healthy controls. electrotransfection was employed to introduce the mir-6747-3p mimic and inhibitor in both HudeP-2 and K562 cells, and red blood cell lineage development was evaluated by ccK-8 assay, flow cytometry, Wright-Giemsa staining and Benzidine blue staining. B-cell lymphoma/leukemia 11a (Bcl11a) was selected as a candidate target gene of mir-6747-3p for further validation through FiSH assay, dual luciferase assay and Western blotting. The results indicated that mir-6747-3p expression was notably higher in patients with β-TM compared with healthy controls and was positively related to HbF levels. Functionally, mir-6747-3p overexpression resulted in the hindrance of cell proliferation, promotion of cell apoptosis, facilitation of cellular erythroid differentiation and γ-globin expression in HudeP-2 and K562 cells. Mechanistically, mir-6747-3p could specifically bind to the 546-552 loci of BCL11A 3'-UTR and induce γ-globin expression. These data indicate that upregulation of mir-6747-3p affects red blood cell lineage development and induces HbF expression by targeting Bcl11a in β-thalassemia, highlighting mir-6747-3p as a potential molecular target for β-thalassemia therapy.

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Up-regulation of microRNA 101-3p during erythropoiesis in β-thalassemia/HbE

Cited by 4 publications

References 43 publications

Clinical implications of miRNAs in erythropoiesis, anemia, and other hematological disorders

Clinical implications of miRNAs in erythropoiesis, anemia, and other hematological disorders

A Review of Key Regulators of Steady-State and Ineffective Erythropoiesis

Upregulation of miR‑6747‑3p affects red blood cell lineage development and induces fetal hemoglobin expression by targeting BCL11A in β‑thalassemia

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