Expression of microRNA-155 in thalassemic erythropoiesis

• DOI: 10.7717/peerj.18054
• Publication Date: 2024-09-20T08:51:36Z
• Authors: Tipparat Penglong; Nuttanan Pholngam; Nasra Tehyoh; Natta Tansila; Hansuk Buncherd; Supinya Thanapong...; Kanitta Srinoun
• Keywords: Erythroblast; Ineffective erythropoiesis; Transferrin receptor

Background Ineffective erythropoiesis (IE) is the primary cause of anemia and associated pathologies in β -thalassemia. The characterization IE imbalance erythroid proliferation differentiation, resulting increased erythroblast that fails to differentiate gives rise enucleate RBCs. MicroRNAs (miRs) are known play important roles hematopoiesis. miR-155 a multifunctional molecule involved both normal pathological hematopoiesis, its upregulation observed patients with -thalassemia/HbE. However, expression function miR-155, especially -thalassemia, have not yet been explored. Methods To study thalassemia, subpopulations, CD45-CD71 + Ter-119 − were collected from IVSII-654 thalassemic bone marrow. Additionally, two-phase culture mouse marrow progenitor cells was performed. Expression predicted mRNA target genes, c-myc , bach-1 pu-1 determined by quantitative reverse transcription (qRT)-polymerase chain reaction (PCR) normalized small nucleolar RNA (snoRNA) 202 glyceraldehyde-3-phosphate dehydrogenase (GAPDH), respectively. investigate effect expression, erythroblasts transfected miR-inhibitor -mimic order elevate eliminate Erythroid cell differentiation evaluated Wright–Giemsa staining flow cytometry. Results upregulated, vivo vitro during -thalassemic mice. Our revealed gain- loss augmented may be upregulation. mice significantly percentage basophilic polychromatic erythroblasts. Conversely, significant decrease anti-miR-155 inhibitor. We also examined targets ( ) which indicated valid gene regulates differentiation. Conclusion -thalassemia via controlling