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Matrix metalloproteinase-9 was involved in the immuno-modulatory defect of mesenchymal stem cell from chronic myeloid leukemia patients 被引量:3

Matrix metalloproteinase-9 was involved in the immuno-modulatory defect of mesenchymal stem cell from chronic myeloid leukemia patients
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摘要 Background Overwhelming evidences on chronic myeloid leukemia (CML) indicate that patients harbor quiescent CML stem cells that are responsible for blast crisis. While the hematopoietic stem cell (HSC) origin of CML was first suggested over 30 years ago, recently CML-initiating cells beyond HSCs are also being investigated. Methods We have previously isolated fetal liver kinase-l-positive (Flkl+) cells carrying the BCR/ABL fusion gene from the bone marrow of Ph+ patients with hemangioblast property. In this study, we isolated CML patient-derived FIk1+CD31-CD34- mesenchymal stem cells (MSCs) and detected their biological characteristics and immunological regulation using fluorescence in situ hybridization (FISH) analysis, fluorescence activated cell sorting (FACS), enzyme-linked immunoadsorbent assay, mixed lymphocyte reaction assays; then we compared these characters with those of the healthy donors. Results CML patient-derived FIk1+CD31-CD34- MSCs had normal morphology, phenotype and karyotype while appeared impaired in immuno-modulatory function. The capacity of patient FIk1+CD31-CD34- MSCs to inhibit T lymphocyte activation and proliferation was impaired in vitro. Conclusions CML patient-derived MSCs have impaired immuno-modulatory functions, suggesting that the dysregulation of hematopoiesis and immune response may originate from MSCs rather than hematopoietic stem cells (HSCs). MSCs might be a potential target for developing efficacious treatment for CML. Background Overwhelming evidences on chronic myeloid leukemia (CML) indicate that patients harbor quiescent CML stem cells that are responsible for blast crisis. While the hematopoietic stem cell (HSC) origin of CML was first suggested over 30 years ago, recently CML-initiating cells beyond HSCs are also being investigated. Methods We have previously isolated fetal liver kinase-l-positive (Flkl+) cells carrying the BCR/ABL fusion gene from the bone marrow of Ph+ patients with hemangioblast property. In this study, we isolated CML patient-derived FIk1+CD31-CD34- mesenchymal stem cells (MSCs) and detected their biological characteristics and immunological regulation using fluorescence in situ hybridization (FISH) analysis, fluorescence activated cell sorting (FACS), enzyme-linked immunoadsorbent assay, mixed lymphocyte reaction assays; then we compared these characters with those of the healthy donors. Results CML patient-derived FIk1+CD31-CD34- MSCs had normal morphology, phenotype and karyotype while appeared impaired in immuno-modulatory function. The capacity of patient FIk1+CD31-CD34- MSCs to inhibit T lymphocyte activation and proliferation was impaired in vitro. Conclusions CML patient-derived MSCs have impaired immuno-modulatory functions, suggesting that the dysregulation of hematopoiesis and immune response may originate from MSCs rather than hematopoietic stem cells (HSCs). MSCs might be a potential target for developing efficacious treatment for CML.
出处 《Chinese Medical Journal》 SCIE CAS CSCD 2011年第16期2423-2430,共8页 中华医学杂志(英文版)
关键词 chronic myeloid leukemia mesenchymal stem cell immune regulation matrix metalloproteinase-9 chronic myeloid leukemia mesenchymal stem cell immune regulation matrix metalloproteinase-9
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