无效红细胞生成是β-地中海贫血的主要原因。无效红细胞生成的关键标志是红细胞的高度增殖。microRNA(miR/miRNA)涉及多个生物学过程,包括细胞增殖和红细胞生成。miR-101被广泛研究并与几种类型的癌症的增殖相关。然而,miR-101-3p尚未在β-地中海贫血/HbE中进行研究。因此,本研究旨在探讨miR-101-3p在β-地中海贫血/HbE红细胞生成过程中的表达。结果显示miR-101-3p在β-地中海贫血/HbE患者的成红细胞在第7天上调,提示miR-101-3p可能与β-地中海贫血/HbE的高增殖有关。因此,研究了miR-101-3p的mRNA靶标,包括Rac1,SUB1,TET2和TRIM44,以确定与β-地中海贫血/HbE成红细胞高增殖相关的机制.与正常对照和轻度β-地中海贫血/HbE相比,重度β-地中海贫血/HbE中的Rac1表达在第11天显著降低。在培养的第9天,重度β-地中海贫血/HbE中的SUB1基因表达明显低于正常对照组。对于TET2和TRIM44表达式,正常和β-地中海贫血/HbE之间未观察到显着差异。然而,miR-101-3p在第7天的高表达与这些靶基因无关,这表明该miRNA可能通过其他靶基因调节β-地中海贫血/HbE的无效红细胞生成。
Ineffective erythropoiesis is the main cause of anemia in β-thalassemia. The crucial hallmark of ineffective erythropoiesis is the high proliferation of erythroblast. microRNA (miR/miRNA) involves several biological processes, including cell proliferation and erythropoiesis. miR-101 was widely studied and associated with proliferation in several types of cancer. However, the miR-101-3p has not been studied in β-thalassemia/HbE. Therefore, this study aims to investigate the expression of miR-101-3p during erythropoiesis in β-thalassemia/HbE. The results showed that miR-101-3p was upregulated in the erythroblast of β-thalassemia/HbE patients on day 7, indicating that miR-101-3p may be involved with high proliferation in β-thalassemia/HbE. Therefore, the mRNA targets of miR-101-3p including Rac1, SUB1, TET2, and TRIM44 were investigated to determine the mechanisms involved with high proliferation of β-thalassemia/HbE erythroblasts. Rac1 expression was significantly reduced at day 11 in severe β-thalassemia/HbE compared to normal controls and mild β-thalassemia/HbE. SUB1 gene expression was significantly lower in severe β-thalassemia/HbE compared to normal controls at day 9 of culture. For TET2 and TRIM44 expression, a significant difference was not observed among normal and β-thalassemia/HbE. However, the high expression of miR-101-3p at day 7 and these target genes was not correlated, suggesting that this miRNA may regulate ineffective erythropoiesis in β-thalassemia/HbE via other target genes.