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骨髓增生异常综合征的发病机制至今尚未明确,有研究表明MDS患者骨髓基质微环境功能的异常与其发病有关。间充质干细胞是造血微环境的重要成分,本研究拟探讨低危MDS患者间充质干细胞(MSC)的生物学特性及功能。采集低危MDS患者的骨髓标本,分离、培养和扩增MSC,观察细胞形态,进行免疫表型、成骨分化能力鉴定,检测其增殖能力及对体外造血的支持功能;用实时定量RT-PCR法测定MSC中相关细胞因子及化学趋化因子的表达,并与健康供者的MSC进行比较。结果表明:培养低危MDS患者的MSC呈典型的成纤维细胞样,细胞表达SH2(CD105),SH3(CD73),Thy-1(CD90),CD34及CD45均为阴性,诱导后可向成骨细胞分化。其体外扩增能力与与健康供者相比无显著差异(p>0.05),但体外支持造血功能较后者显著减低(p<0.05)。实时定量PT-PCR显示SDF-1基因在低危MDS患者MSC中显著高表达(p<0.01)。结论:间充质干细胞的功能异常与低危MDS患者骨髓微环境的造血调控失常相关,这为MDS发病机制的认识及治疗提供了新的思路,值得进一步探讨。
The pathogenesis of myelodysplastic syndrome is still not clear, some studies have shown that abnormalities of bone marrow microenvironment in MDS patients with its pathogenesis. Mesenchymal stem cells are an important component of hematopoietic microenvironment. This study was to investigate the biological characteristics and function of mesenchymal stem cells (MSCs) in patients with low-risk MDS. Bone marrow samples of low-risk MDS patients were collected, MSC were isolated, cultured and expanded to observe the cell morphology, immunophenotype, identification of osteogenic differentiation ability, detection of its proliferation and hematopoietic function in vitro; real-time quantitative RT-PCR Method to determine the expression of related cytokines and chemokines in MSC and compare them with that of healthy donors. The results showed that the MSCs cultured in low-risk MDS showed typical fibroblast-like morphology. The expression of SH2 (CD105), SH3 (CD73), Thy-1 (CD90), CD34 and CD45 were all negative. Cell Differentiation. There was no significant difference (p> 0.05) between the in vitro expansion ability and the healthy donors, but the hematopoietic function in vitro was significantly lower than that of the latter (p <0.05). Real-time quantitative PT-PCR showed that SDF-1 gene was highly expressed in MSC of low-risk MDS patients (p <0.01). CONCLUSION: The dysfunction of mesenchymal stem cells is associated with disorders of hematopoietic regulation of bone marrow microenvironment in low-risk MDS patients, which provides a new idea for understanding and treating the pathogenesis of MDS and deserves further exploration.