吴克复
七十年代建立人白血病细胞系填补国内空白。八十年代从事抑制因子研究发现人成纤维细胞产生肿瘤抑制因子和白血病细胞增殖抑制因子。九十年代对膜结合因子的接触性调节进行分析
个性化签名
- 姓名:吴克复
- 目前身份:
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学术头衔:
博士生导师
- 职称:-
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学科领域:
病理学
- 研究兴趣:七十年代建立人白血病细胞系填补国内空白。八十年代从事抑制因子研究发现人成纤维细胞产生肿瘤抑制因子和白血病细胞增殖抑制因子。九十年代对膜结合因子的接触性调节进行分析
1964年毕业于中国协和医科大学,一直在中国医学院下属研究所从事基础医学研究。七十年代建立人白血病细胞系填补国内空白。八十年代从事抑制因子研究发现人成纤维细胞产生肿瘤抑制因子和白血病细胞增殖抑制因子。九十年代对膜结合因子的接触性调节进行分析。近五年来对细胞间通讯的其他方面(离子通道等)与白血病肿瘤的关系进行研究。
曾担任十余项国家研究项目,获卫生部科技进步奖一等奖一项、二等奖二项、中华医学奖二等奖一项。发表论文一百多篇,培养硕士8名、博士12名
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吴克复
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-1年11月30日
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吴克复
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-1年11月30日
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【期刊论文】Clone and expression of mutant M-CSF and its receptor from human leukemic cell line J6-1
吴克复
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-1年11月30日
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吴克复
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-1年11月30日
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吴克复, QING RAO, GUO-GUANG ZHENG, GE LI, YONG-MIN LIN, AND KE-FU WU
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-1年11月30日
Earlier studies indicate that J6-1 human leukemic cells proliferate and propagate via the membrane-bound macrophage colony-stimulating factor (M-CSF)-mediated auto-juxtacrine mechanism. Matrix metalloproteinases (MMPs) can modulate the activity of cell membrane molecules and influence many cellular behaviors. Therefore, we hypothesized that MMP may also be involved in the membrane-bound M-CSF-mediated juxtacrine mechanism. First, we investigated whether blocking of membrane-bound M-CSF by neutralizing antibody to M-CSF or M-CSF receptor and adding of exogenous M-CSF are able to influence MMP-9 release. Next, we determined whether MMP-9 participated in J6-1 cells proliferation and influence the shedding of membrane-bound M-CSF and its receptor. Current studies show that blockade of the interaction between membrane-bound M-CSF and M-CSF receptor by antibody to M-CSF or M-CSF receptor promotes MMP-9 release. Moreover, we demonstrated that because of M-CSF mediated juxtacrine, lack of MMP-9 promotes J6-1 cell proliferation, in which a decrease in the shedding of cell-surface M-CSFR is involved. Hence, we suggest that membrane-bound M-CSF inhibit MMP-9 release and down-regulated MMP-9 contribute to juxtacrine stimulating in leukemic cell growth.
human leukemia, macrophage colony-stimulating factor, matrix metalloproteinase-9, juxtacrine, soluble receptor, shedding
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吴克复, B Zhang, K-F Wu, Y-M Lin, X-T Ma, Q Rao, G-G Zheng, Z-Y Cao, G Li and Y-H Song
Leukemia(2004), 1-9,-0001,():
-1年11月30日
We report in a murine model of acute lymphoid leukemia L1210 the potent antitumor efficiency of a combinatorial delivery of pro-IL-18 gene modified L1210 (Lp18) and IL-1b converting enzyme (ICE) gene modified L1210 (LpICE). Live leukemia cells Lp18 or Lp18 plus LpICE showed apparently reduced leukemogenicity with a survival rate of 40 or 50% at 50 days after intraperitoneal (i.p.) inoculation of a lethal dose of cells, respectively. Combination of Lp18 and LpICE was capable of inhibiting accumulation of bloody ascites, synergistically superior to Lp18 or LpICE alone. All surviving mice were rechallenged with parental L1210 cells at day 50, and all survived up to day 80, suggesting that gene-modified cells induced immune protection. Moreover, NK cytotoxicity and CTL activity were both enhanced in mice injected with Lp18, especially Lp18 plus LpICE. Levels of IFN-c were not altered significantly by inoculation of Lp18 or Lp18 plus LpICE. Our results demonstrate that IL-18 is a useful candidate gene in gene therapy of lymphoma or lymphoid leukemia, and ex vivo combinatorial delivery of Lp18 plus LpICE either as a single approach or as an adjunct to concomitant radiotherapy or chemotherapy, may be more efficient in a situation of minimal residual disease.
interleukin 18, ICE, gene modified, L1210, antitumor effects, immunotherapy
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吴克复, Xiao-Tong Ma, Xiu-Jun Zhang, Bin Zhang, Yi-Qi Geng, Yong-Min Lin, Ge Li, Ke-Fu Wu*
Cell Biology International 28(2004)689-697,-0001,():
-1年11月30日
IL-23 is a novel cytokine composed of an IL-12 p40 and a p19 subunit. We analyzed human peripheral blood mononuclear cells (PBMC) and hematopoietic cell lines for constitutive expression of IL-23 and IL-12 subunits and expression following exposure to various stimuli, and investigated the mechanisms of their induction by LPS and SAC. IL-23 p19 and IL-12 p35 mRNAs were expressed in fresh PBMC, and expression of all IL-23 and IL-12 subunits was up-regulated by LPS and SAC. LPS-induced increase of IL-23 and IL-12 subunits expression was CD14-dependent, while CD14 was not involved in SAC-induced p19 transcription. Both LPS-and SAC-induced subunits expression required p38 MAPK pathway. PHA effected an increase of p19 mRNA in both CD4C and CD8C T cells, whereas p35 was minimally regulated by PHA. IFN-g primed monocytes for LPS stimulation of p19, p35 and p40 expression. p19 mRNA was detectable in most hematopoietic cell lines tested but p35 distribution was more restricted. A phorbol diester enhanced p19, p35 and p40 expression in EBV-positive cell lines. Our results suggest that both the subunits of IL-23 are tightly regulated; the expression pattern and regulation mode of IL-23 p19 is similar to as well as distinct from that of IL-12 p35.
Interleukin-23, Interleukin-12, Bacteria and bacterial product, Signal transduction
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