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正常骨髓基质细胞对K562细胞凋亡敏感性的影响 被引量:1

Effects and mechanisms of bone marrow stromal cells on apoptotic sensitivity of leukemia cell line K562
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摘要 目的观察正常人骨髓基质细胞对白血病敏感细胞株K562细胞凋亡易感性的影响,并研究其作用机制。方法建立正常人骨髓基质细胞的体外培养体系及其与K562细胞共培养的体系;流式细胞仪检测Annexin V阳性的早期凋亡细胞;电镜下观察凋亡形态学改变;流式细胞仪检测bcl-2,活化的胱冬氨酸蛋白酶(caspaae)-3的表达变化。结果与单独K562细胞培养相比,与正常人骨髓基质细胞共培养的K562细胞,分别经阿糖胞苷作用后,共培养体系下其凋亡率下降,电镜下细胞凋亡的形态改变减少或消失,而且bcl-2蛋白表达上调,活化的caspase-3表达减弱。结论正常人骨髓基质细胞可促进白血病细胞株K562细胞的增殖,降低K562细胞对阿糖胞苷的凋亡易感性,其作用机制中包括影响凋亡相关蛋白bcl-2和caspase-3的表达。 Objective To investigate the effects and mechanisms of the normal bone marrow stromal cells (BMSCs) on chemosensitivity of K562 cell line in vitro. Methods Culture system of BMSCs and co-culture system of K562 cells and BMSCs in vitro were established. Expressions of active caspase-3 and bcl-2 were detected by flow cytometry using Annexin V FIFC staining; morphological assessment of apoptosis was performed with transmission electron microscope. Results Compared with K562 cells treated by Ara-C without BMSCs, the percentage of Annexin V-positive cells, apoptotic ratio, apoptotic morphological changes, and the expression of active caspase-3 decreased while bcl-2 increased in K562 cells treated by Ara-C co-cultured with BMSCs. Conclusion Normal bone marrow stromal cells can promote the proliferation of K562 cells, prevent Ara-C-induced apoptosis in K562 cells via modulation of bcl-2 and active caspase-3.
出处 《兰州大学学报(医学版)》 CAS 2007年第2期1-4,9,共5页 Journal of Lanzhou University(Medical Sciences)
关键词 正常骨髓基质细胞 白血病 凋亡 K562细胞 normal bone marrow stromal cells leukemia apoptosis K562 cell
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参考文献9

  • 1[1]MATSUNAGA T,TAKEMOTO N,SATO T,et al.Interaction between leukemic-cell VLA-4 and stromal fibronectin is a decisive factor for minimal residual dis ease of acutemyelogenous leukemia[J].National Medicine,2003,9(9):1 158-1 165.
  • 2[2]PETRUSCA D N,PETRESCU A,VRABIE C,et al.Cell cycle regulatory factors in juxtatumoral renal parenchyma[J].Cell Death Differ,2005,46(2):117-22.
  • 3[3]FORTNEY J E,ZHAO W,WENGER S L,et al.Bone marrow stromal cells regulate caspaee 3 activity in leukemic cells during chemotherapy[J].Leuk Research,2001,25(10):901-907.
  • 4许贞书,刘拥军,吕璐璐,韩之波,王彤,陈志哲,韩忠朝.基质细胞抑制HL-60细胞凋亡机制初探[J].中华血液学杂志,2005,26(6):375-377. 被引量:1
  • 5[6]GIBSON L F.Survival of B lineage leukemic cells:signals from the bone marrow microenvironment[J].Leuk Lymphoma,2002,43 (1):19-27.
  • 6[7]GRANZIERO L,CIRCOSTA P,SCIELZO C,et al.CD100 /PlexinOB1 interac-tions sustain prollferation and survival of normal and leukemic CD5+B lymphocytes[J].Blood,2003,101(5):1 962-1 969.
  • 7[8]PARAGUASSU B F H,BOROJEVIC R,BOUZAS L F,et al.Bone marrow stroma inhibits proliferation and apoptosis in leukemic cells through gap junction mediated cell communication[J].Cell Death Differ,2003,10(9):1 101-1 108.
  • 8[9]NEFEDOVA Y,LANDOWSKI T H,DOLTON W S.Bone marrow stromal-derived soluble factors and direct cell contact contribute to de novo drug resistance ofnyeloma cells by distinct mechanisms[J].Leukemia,2003,17(16):1 175-1 182.
  • 9李忠俊,滕本秀,陈幸华,孔佩艳,王吉刚,彭贤贵,杨镇洲.白血病骨髓基质细胞对白血病细胞屏蔽效应的体外实验研究[J].癌症,2005,24(6):672-675. 被引量:9

二级参考文献15

  • 1Shimakura Y, Kawada H, Ando K, et al. Murine stromal cell line Hess-5 maintains reconstituting ability of ex vivo-generated hematopoietic stem cells from human bone marrow and cytokine-mobilized peripheral blood. Stem Cells, 2000, 18: 183-189.
  • 2Konopleva M, Konoplev S, Hu W, et al. Stromal cells prevent apoptosis of AML cells by up-regulation of anti-apoptotic proteins. Leukemia, 2002, 16: 1713-1724.
  • 3Goulden N,Langlands K,Seward C,et al.PCR assessment of bone marrow status in "isolated" extramedullary relapse of childhood B-precursor acute lymphoblastic leukaemia. Br J Haematol, 1994, 87:282-285.
  • 4Shah N, Oseth L,leBien TW.Development of a model for evaluating the interaction between human pre-B acute lymphoblastic leukemia cells and the bone marrow stromal cell microenvironment. Blood,1998, 92 : 3817-3828.
  • 5Granziero L, Circosta P, Scielzo C, et al. CD100/Plexin-B1 interactions sustain proliferation and survival of normal and leukemic CD5+ B lymphocytes[J]. Blood, 2003,101 (5):1962-1969.
  • 6Matsunaga T, Takemoto N, Sato T, et al. Interaction between leukemic-cell VLA-4 and stromal fibronectin is a decisive factor for minimal residual disease of acute myelogenous leukemia[J]. Nat Med, 2003,9(9): 1158-1165.
  • 7Jin H J, Chen J, Karageorgiou V, et al. Human bone marrow stromal cell responses on electrospun silk fibroin mats[J].Biomaterials, 2004,25(26): 1039-1047.
  • 8Gibson LF. Survival of B lineage leukemic cells: signals from the bone marrow microenvironment[J]. Leuk Lymphoma,2002,43(1): 19-27.
  • 9Paraguassu-Braga FH, Borojevic R, Bouzas LF, et al. Bone marrow stroma inhibits proliferation and apoptosis in leukemic cells through gap junction-mediated cell communication[J].Cell Death Differ, 2003,10(9): 1101-1108.
  • 10Lagneaux L, Delforge A, Bron D, et al. Chronic lymphocytic leukemic B cells but not normal B cells are rescued from apoptosis by contact with normal bone marrow stromal cells[J]. Blood, 1998,91(7):2387-2396.

共引文献8

同被引文献7

  • 1李忠俊,滕本秀,陈幸华,孔佩艳,王吉刚,彭贤贵,杨镇洲.白血病骨髓基质细胞对白血病细胞屏蔽效应的体外实验研究[J].癌症,2005,24(6):672-675. 被引量:9
  • 2Hussein M A, Juturi JV, Lieberman I. Multiple myeloma: present and future [J]. Curr Opin Oncol, 2002;14( 1 ) :31-35.
  • 3Nefedova Y, Landowski T H, Dalton W S. Bone marrow strornal-derived soluble factors and direct cell contact contribute to de novo drug resistance of myeloma cells by distinct mechanisms [ J ]. Leukemia, 2003 ; 17 (6) :1175-1182.
  • 4Vanderslice P, Biediger R J, Woodside DG, et al. Development of cell adhesion molecule antagonists as therapeutics for asthma and COPD [J]. Pulm Pharmacol Ther, 2004;17(1) :1-10.
  • 5Mahlknecht U, Sch6nbein C. Histone deaeetylase inhibitor treatment downregulates VLA-4 adhesion in hematopoietic stem cells and acute myeloid leukemia blast cells [ J ]. Haematologica, 2008; 93 (3) :443-447.
  • 6Moshaver B, van der Pol MA, Westra AH, et al. Chemotherapeutic treatment of bone marrow stromal cells strongly affects their protective effect on acute myeloid leukemia cell survival [J]. Leuk Lymphoma, 2008;49(1 ) :134-148.
  • 7Matsunaga T, Takemoto N, Sato T, et al. Interaction between leukemic cell VLA-4 and stromal fibronectin is a decisive factor for minimal residual disease of acute myelogenons leukemia [J]. Nat Med, 2003 ; 9(9) :1158-1165.

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