Downregulation of extracellular vesicle microRNA-101 derived from bone marrow mesenchymal stromal cells in myelodysplastic syndrome with disease progression.
Downregulation of extracellular vesicle microRNA-101 derived from bone marrow mesenchymal stromal cells in myelodysplastic syndrome with disease progression.
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DOI：
10.3892/ol.2020.11282
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发表时间：
2020-03
期刊：
影响因子：
2.9
通讯作者：
Y. Saitoh;Tomohiro Umezu;S. Imanishi;M. Asano;S. Yoshizawa;S. Katagiri;T. Suguro;Hiroaki Fujimoto;D. Akahane;Chiaki Kobayashi-Kawana;J. Ohyashiki;K. Ohyashiki
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文献类型：
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作者：
Y. Saitoh;Tomohiro Umezu;S. Imanishi;M. Asano;S. Yoshizawa;S. Katagiri;T. Suguro;Hiroaki Fujimoto;D. Akahane;Chiaki Kobayashi-Kawana;J. Ohyashiki;K. Ohyashiki
为探讨骨髓恶性肿瘤与骨髓微环境细胞之间的相互作用机制，本研究建立了骨髓间充质基质细胞（MSCs），并检测了22例骨髓增生异常综合征（MDS）和7例急性髓性白血病伴骨髓增生异常相关改变（AML/MRC）患者的细胞外囊泡（EV）microRNA（miR）表达。根据修订的国际预后评分系统（IPSS-R）将MDS患者分为两类，并使用TaqMan低密度阵列评估BM-MSCs中EV-miR的表达。使用逆转录-定量PCR评估所选择的miR。目前的研究表明，BM-MSC衍生的EV-miR的表达是异质性的，并且基于MDS的严重程度，与对照组和低风险组相比，高危组和AML/MRC患者中EV-miR-101的表达较低。这与BM原始细胞百分比可逆相关，来自BM-MSC的细胞miR-101或血清EV-miR-101表达与BM原始细胞百分比没有关联。数据库分析表明，miR-101负调控细胞增殖和表观遗传基因表达。BM-MSC衍生的EV-miR-101的下调可能与细胞间通讯相关，并可能加速MDS细胞的恶性过程。
To evaluate the mechanism underlying the communication between myeloid malignant and bone marrow (BM) microenvironment cells in disease progression, the current study established BM mesenchymal stromal cells (MSCs) and assessed extracellular vesicle (EV) microRNA (miR) expression in 22 patients with myelodysplastic syndrome (MDS) and 7 patients with acute myeloid leukemia and myelodysplasia-related changes (AML/MRC). Patients with MDS were separated into two categories based on the revised International Prognostic Scoring System (IPSS-R), and EV-miR expression in BM-MSCs was evaluated using a TaqMan low-density array. The selected miRs were evaluated using reverse transcription-quantitative PCR. The current study demonstrated that the expression of BM-MSC-derived EV-miR was heterogenous and based on MDS severity, the expression of EV-miR-101 was lower in high-risk group and patients with AML/MRC compared with the control and low-risk groups. This reversibly correlated with BM blast percentage, with which the cellular miR-101 from BM-MSCs or serum EV-miR-101 expression exhibited no association. Database analyses indicated that miR-101 negatively regulated cell proliferation and epigenetic gene expression. The downregulation of BM-MSC-derived EV-miR-101 may be associated with cell-to-cell communication and may accelerate the malignant process in MDS cells.