再障骨髓间充质干细胞的异常及其基因表达谱的改变
再生障碍性贫血（AA）患者的除骨髓造血干细胞有缺陷，T细胞免疫功能异常外，其骨髓间充质干细胞也被证明存在着基因表达和生物学功能的异常，提示AA的骨髓造血微环境破灭，可能是因为相关基因表达谱的改变造成的。
延伸： AA通常是一种自身免疫性疾病，其造血干细胞与造血微环境的缺陷理论上可以通过同时移植造血干细胞和间充质干细胞得到治疗，且间充质干细胞的独特的免疫调节功能使其在AA治疗中颇具前景。
3. PLoS One. 2012;7(11):e47764. doi: 10.1371/journal.pone.0047764. Epub 2012 Nov 5.
Differential gene expression profile associated with the abnormality of bone marrow mesenchymal stem cells in aplastic anemia.
Li J, Yang S, Lu S, Zhao H, Feng J, Li W, Ma F, Ren Q, Liu B, Zhang L, Zheng Y, Han ZC.
Source
State Key Laboratory of Experimental Hematology, Institute of Hematology and Hospital of Blood Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin, China.
Abstract
Aplastic anemia (AA) is generally considered as an immune-mediated bone marrow failure syndrome with defective hematopoietic stem cells (HSCs) and marrow microenvironment. Previous studies have demonstrated the defective HSCs and aberrant T cellular-immunity in AA using a microarray approach. However, little is known about the overall specialty of bone marrow mesenchymal stem cells (BM-MSCs). In the present study, we comprehensively compared the biological features and gene expression profile of BM-MSCs between AA patients and healthy volunteers. In comparison with healthy controls, BM-MSCs from AA patients showed aberrant morphology, decreased proliferation and clonogenic potential and increased apoptosis. BM-MSCs from AA patients were susceptible to be induced to differentiate into adipocytes but more difficult to differentiate into osteoblasts. Consistent with abnormal biological features, a large number of genes implicated in cell cycle, cell division, proliferation, chemotaxis and hematopoietic cell lineage showed markedly decreased expression in BM-MSCs from AA patients. Conversely, more related genes with apoptosis, adipogenesis and immune response showed increased expression in BM-MSCs from AA patients. The gene expression profile of BM-MSCs further confirmed the abnormal biological properties and provided significant evidence for the possible mechanism of the destruction of the bone marrow microenvironment in AA.
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