Objective To isolate mesenchymal stem cells(MSCs)from human umbilical cord and investigate the basic biological characteristics.Methods Human umbilical cord mesenchymal stem cells(hUCMSCs)were separated from culture o...Objective To isolate mesenchymal stem cells(MSCs)from human umbilical cord and investigate the basic biological characteristics.Methods Human umbilical cord mesenchymal stem cells(hUCMSCs)were separated from culture of tissue adherence and the biological characteristics,including morphologic appearance,surface antigens,growth curve,cell cycle,cytogenetic features,differentiation potential and gene expression,were investigated.Results After two weeks of incubation,fibroblast-like cells appeared to be dominant.During the second passage the cells presented a homogeneous population of spindle fibroblast-like cells.Flow cytometry analysis revealed that CD29,CD44,CD95,CD105 and HLA-I were expressed on the surface of cells,but there was no expression of hematopoietic lineage markers,e.g.,CD34,CD38,CD71 and HLA-DR.Chromosomal analysis showed the cells kept normal karyotype.The cell cycle at the third passage showed the percentage of G0/G1,G2/M and S phase were 88.86%,5.69% and 5.45% respectively.The assays in vitro demonstrated the cells exhibited multipotential differentiation into osteogenic and adipogenic cells.Both BMI-1 and nucleostemin genes,expressed in adult MSCs from bone marrow,were also expressed in hUCMSCs.Conclusion Here we show the umbilical cords may be a novel alternative source of human MSCs for experimental and clinical applications,which almost have the same biological characteristics of human adult MSCs.展开更多
背景:F-Box和WD40蛋白7(F-Box and WD40 domain protein 7,FBXW7)是E3泛素连接酶复合物的组份,控制NOTCH1,c-MYC和Cyclin E等多种蛋白的降解。目的:研究成人T细胞性急性淋巴细胞白血病(T-ALL)中FBXW7基因突变。方法:通过对54例成人T-AL...背景:F-Box和WD40蛋白7(F-Box and WD40 domain protein 7,FBXW7)是E3泛素连接酶复合物的组份,控制NOTCH1,c-MYC和Cyclin E等多种蛋白的降解。目的:研究成人T细胞性急性淋巴细胞白血病(T-ALL)中FBXW7基因突变。方法:通过对54例成人T-ALL患者FBXW7外显子5-12进行扩增、克隆和测序,分析FBXW7突变的发生率、突变位点和类型、与NOTCH1突变的相关性及其临床预后意义。结果:本组成人T-ALL中FBXW7突变率11.1%,共发现4种点突变(R465H,R465L,R479P和R505C)和1个插入/缺失突变,FBXW7突变全部位于WD40结构域。研究还发现,FBXW7突变患者中83.3%同时存在NOTCH1突变,与FBXW7突变并存的NOTCH1突变均发生于HD结构域,包括点突变(L1574P,L1596H和L1600P),和缺失/插入突变。此外,研究还显示,FBXW7单独突变组患者的总生存时间比无突变组延长(P=0.049)。结论:FBXW7突变可能在NOTCH1介导的TALL发病机制有重要作用。展开更多
文摘Objective To isolate mesenchymal stem cells(MSCs)from human umbilical cord and investigate the basic biological characteristics.Methods Human umbilical cord mesenchymal stem cells(hUCMSCs)were separated from culture of tissue adherence and the biological characteristics,including morphologic appearance,surface antigens,growth curve,cell cycle,cytogenetic features,differentiation potential and gene expression,were investigated.Results After two weeks of incubation,fibroblast-like cells appeared to be dominant.During the second passage the cells presented a homogeneous population of spindle fibroblast-like cells.Flow cytometry analysis revealed that CD29,CD44,CD95,CD105 and HLA-I were expressed on the surface of cells,but there was no expression of hematopoietic lineage markers,e.g.,CD34,CD38,CD71 and HLA-DR.Chromosomal analysis showed the cells kept normal karyotype.The cell cycle at the third passage showed the percentage of G0/G1,G2/M and S phase were 88.86%,5.69% and 5.45% respectively.The assays in vitro demonstrated the cells exhibited multipotential differentiation into osteogenic and adipogenic cells.Both BMI-1 and nucleostemin genes,expressed in adult MSCs from bone marrow,were also expressed in hUCMSCs.Conclusion Here we show the umbilical cords may be a novel alternative source of human MSCs for experimental and clinical applications,which almost have the same biological characteristics of human adult MSCs.
文摘背景:F-Box和WD40蛋白7(F-Box and WD40 domain protein 7,FBXW7)是E3泛素连接酶复合物的组份,控制NOTCH1,c-MYC和Cyclin E等多种蛋白的降解。目的:研究成人T细胞性急性淋巴细胞白血病(T-ALL)中FBXW7基因突变。方法:通过对54例成人T-ALL患者FBXW7外显子5-12进行扩增、克隆和测序,分析FBXW7突变的发生率、突变位点和类型、与NOTCH1突变的相关性及其临床预后意义。结果:本组成人T-ALL中FBXW7突变率11.1%,共发现4种点突变(R465H,R465L,R479P和R505C)和1个插入/缺失突变,FBXW7突变全部位于WD40结构域。研究还发现,FBXW7突变患者中83.3%同时存在NOTCH1突变,与FBXW7突变并存的NOTCH1突变均发生于HD结构域,包括点突变(L1574P,L1596H和L1600P),和缺失/插入突变。此外,研究还显示,FBXW7单独突变组患者的总生存时间比无突变组延长(P=0.049)。结论:FBXW7突变可能在NOTCH1介导的TALL发病机制有重要作用。
