MiR-155 enhances phagocytic activity of β-thalassemia/HbE monocytes via targeting of BACH1
Autor: | Malai Wongchanchailert, Chamnong Nopparatana, Suthat Fucharoen, Kanitta Srinoun |
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Rok vydání: | 2017 |
Předmět: |
Adult
Male 0301 basic medicine congenital hereditary and neonatal diseases and abnormalities medicine.medical_specialty Adolescent Phagocytosis Monocytes miR-155 03 medical and health sciences Downregulation and upregulation hemic and lymphatic diseases Internal medicine parasitic diseases medicine Humans Regulation of gene expression Hematology Chemistry Hemoglobin E Monocyte beta-Thalassemia virus diseases digestive system diseases MicroRNAs Red blood cell Basic-Leucine Zipper Transcription Factors 030104 developmental biology medicine.anatomical_structure Gene Expression Regulation Immunology Female |
Zdroj: | International Journal of Hematology. 106:638-647 |
ISSN: | 1865-3774 0925-5710 |
Popis: | Abnormal red blood cell (RBC) clearance in β-thalassemia is triggered by activated monocytes. Recent reports indicate that miRNA (miR-) plays a role in monocyte activation. To study phagocytic function, we co-cultured monocytes of normal, non-splenectomized and splenectomized β-thalassemia/HbE individuals with RBCs obtained from normal, non-splenectomized and splenectomized β-thalassemia/HbE individuals. The phagocytic activity of β-thalassemia/HbE monocytes co-cultured with β-thalassemia/HbE RBCs was significantly higher than that of normal monocytes co-cultured with normal RBCs. Upregulation of monocyte miR-155 was observed in β-thalassemia/HbE patients. Increased miR-155 was associated with reductions in BTB and CNC Homology1 (BACH1) target gene expression and increased phagocytic activity of β-thalassemia/HbE monocytes. Taken together, these findings suggested that increased miR-155 expression in activated monocytes leads to enhanced phagocytic activity via BACH-1 regulation in β-thalassemia/HbE. This provides novel insights into the phagocytic clearance of abnormal RBCs in β-thalassemia/HbE. |
Databáze: | OpenAIRE |
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