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Acta Biochimica et Biophysica Sinica 2004年第6期36卷 425-429页

作者： Ji-Hong WANG, Yu WU, Feng REN, Li Lü, and Bao-Chang ZHAO*Department of Biochemistry and Molecular Biology, Dalian Medical University, Dalian 116027, China Department of Biochemistry and Molecular Biology Dalian Medical UniversityDalian 116027 China

Adinbitor was cloned from Agkistrodon halys brevicaudus stejneger and characterized as a novel disintegrin. In this study, total RNA was extracted from venom gland and used in RT-PCR to generate a cDNA which is 219 bp long. The sequence encoded a polypeptide composed of 73 amino acids, including 12 cysteines, an RGD motif, and the signature motif of disintergrin. Recombinant Adinbitor (rAdinbitor) was expressed in E. coli and purified by using the His?Bind affinity chromatography. The IC50 for inhibiting human platelet aggregation and bFGF-induced proliferation of ECV304 cells was 6 μΜ and 0.89 μΜ respectively. Furthermore, Adinbitor significantly inhibited angiogenesis both in vivo and in vitro. Taken together, these results suggested that Adinbitor had typical functions of disintegrins.

关键词： cloning Adinbitor disintegrin platelet aggregation angiogenesis

rAdinbitor, a novel disintegrin from Agkistrodon halys brevicaudus stejneger inhibits adhesion and proliferation of SMMC-7721 cells

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The Chinese-German Journal of Clinical Oncology 2008年第7期7卷 390-393页

作者： Chunling Zhao Xiuyun Cui Feng Ren Baochang Zhao Department of Biochemical and Molecular Biology Dalian Medical University Dalian 116027 China

Objective： To investigate the effects of rAdinbitor on the adhesion and proliferation of human hepatoma cell strain 8MMC-7721. Methods： Cell adhesion assay was used to observe the effect of rAdinbitor on the adhesion of 8MMC-7721 cells to fibronectin （FN）. Crystal violet staining was performed to detect the influence of rAdinbitor on the adhesion of 8MMC- 7721 cells. MTT assay was employed to detect the inhibitory effects of different concentration of rAdinbitor on the proliferation of 8MMC-7721 cells. The morphologic changes of the control 8MMC-7721 cells and the apoptotic cells induced by 200μg/mL rAdinbitor for 36 h were observed under light microscope after HE staining. Flow cytometry analysis was applied to determine the apoptosis rate of 8MMC-7721 cells. Results：（1） FN promoted the adhesion of human hepatoma cell strain 8MMC-7721 in a dose-dependent manner. （2） rAdinbitor could dose-dependently inhibit the adhesion of SMMC-7721 cells to FN. The higher the concentration was, the stronger the inhibition was. There was significant difference among the groups （P 〈 0.05）. （3） rAdinbitor had a strong inhibition on the proliferation of 8MMC-7721 cells and showed a dose-dependent manner （P 〈 0.05）. After a 48 h exposure, the IC50 value of rAdinbitor was 177.83 μg/mL. （4） After exposure of 8MMC-7721 cells to 200μg/mL rAdinbitor for 36 h, the early morphologic changes appeared and the apoptosis rate was 20.68%, significantly higher than that of the control group （2.38%, P 〈 0.05）. Conclusion： rAdinbitor can dose-dependently inhibit the 8MMC-7721 cells adhesion to FN, and can inhibit the proliferation in dose-dependent manner and promote their apoptosis.

关键词： rAdinbitor disintegrin hepatoma adhesion proliferation apoptosis

慢病毒介导的解整合素-金属蛋白酶17RNA干扰对气道上皮细胞MMP-9表达及NF-κB活性的影响

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中国药理学通报 2014年第4期30卷 559-565页

作者：严建平李亚清钟晖陈淳顾超浙江省人民医院呼吸内科浙江杭州310014

目的探讨脂多糖(LPS)诱导的气道上皮细胞基质金属蛋白酶9(MMP-9)表达的TNF-α/NF-κB信号转导机制及慢病毒介导的解整合素-金属蛋白酶17(ADAM17)RNA干扰(RNAi)对MMP-9表达的影响。方法构建ADAM17 siRNA慢病毒载体、包装重组慢病毒。以NF... 详细信息

目的探讨脂多糖(LPS)诱导的气道上皮细胞基质金属蛋白酶9(MMP-9)表达的TNF-α/NF-κB信号转导机制及慢病毒介导的解整合素-金属蛋白酶17(ADAM17)RNA干扰(RNAi)对MMP-9表达的影响。方法构建ADAM17 siRNA慢病毒载体、包装重组慢病毒。以NF-κB抑制剂(pyrrolidine dithiocarbamate,PDTC)或TNF-α拮抗剂(etanercept)预处理HBE4-E6/E7细胞,以LPS刺激HBE4-E6/E7细胞24 h。以重组慢病毒感染HBE4-E6/E7细胞72 h后,以LPS或TNF-α刺激HBE4-E6/E7细胞24 h。以半定量RT-PCR检测MMP-9 mRNA表达;以酶联免疫吸附试验检测TNF-α蛋白含量;以Western blot检测MMP-9蛋白表达;以凝胶阻滞分析实验检测NF-κB活性。结果 LPS或TNF-α刺激均明显增加HBE4-E6/E7细胞MMP-9 mRNA和蛋白表达及NF-κB活性(P0.05)。PDTC明显抑制TNF-α诱导的MMP-9 mRNA和蛋白表达及NF-κB活性(P<0.05)。结论 TNF-α/NF-κB信号通路参与调控LPS诱导的气道上皮细胞MMP-9的表达,ADAM17通过调节TNF-α释放在其信号通路上游起到重要作用。

关键词： RNA干扰慢病毒气道上皮细胞解整合素-金属蛋白酶17 基质金属蛋白酶肿瘤坏死因子-α a disintegrin and metalloproteinase 17 tumor necrosis factor-α

ADAM9特异性siRNA对肾透明细胞癌786-0细胞ADAM9基因表达及体外侵袭能力的影响

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郑州大学学报（医学版） 2014年第1期49卷 59-62页

作者：张新恒马曜辉单中杰新乡医学院研究生处新乡473003 郑州人民医院泌尿外科郑州450003

目的:探讨去整合素金属蛋白酶9(ADAM9)特异性siRNA对人肾透明细胞癌(RCCC)786-0细胞中ADAM9基因表达及体外侵袭能力的影响。方法:设计合成ADAM9特异性siRNA。将786-0细胞分4组处理,分别为正常对照组(正常培养786-0细胞)、空脂质体转染... 详细信息

目的:探讨去整合素金属蛋白酶9(ADAM9)特异性siRNA对人肾透明细胞癌(RCCC)786-0细胞中ADAM9基因表达及体外侵袭能力的影响。方法:设计合成ADAM9特异性siRNA。将786-0细胞分4组处理,分别为正常对照组(正常培养786-0细胞)、空脂质体转染组、阴性转染组(转染无义siRNA)和ADAM9 siRNA转染组。转染24、48、72 h后,采用RT-PCR法检测细胞ADAM9 mRNA的表达;转染48 h后,采用Western blot法检测细胞ADAM9蛋白的表达,并用Transwell法检测细胞侵袭能力。结果:转染24、48、72 h后,ADAM9 siRNA转染组786-0细胞ADAM9 mRNA的表达显著低于其他3组(F=47.945、180.456、60.978,P均<0.001);转染48 h后,ADAM9 siRNA转染组786-0细胞ADAM9蛋白表达显著降低(F=142.816,P<0.001),穿膜细胞数显著减少(F=45.389,P<0.001)。结论:ADAM9特异性siRNA能够有效沉默786-0细胞中ADAM9的表达并降低其体外侵袭能力。

关键词：肾透明细胞癌去整合素金属蛋白酶9 侵袭 a disintegrin and metalloprotease 9

内蒙古地区蒙古族ADAM33基因多态性与COPD易感性的研究

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内蒙古医科大学学报 2014年第2期36卷 119-124页

作者：覃洁白云飞孙超崔丽英内蒙古医科大学附属医院内蒙古呼和浩特010050 内蒙古医科大学第二附属医院

目的:了解内蒙古地区蒙古族人类解整连蛋白和金属蛋白(A disintegrin and metalloproteinase 33,ADAM33)基因单核苷酸多态性与慢性阻塞性肺疾病(COPD)的相关性。方法:采用引物序列特异性聚合酶链反应—限制性片段长度多态性(PCR-RFLP)方... 详细信息

目的:了解内蒙古地区蒙古族人类解整连蛋白和金属蛋白(A disintegrin and metalloproteinase 33,ADAM33)基因单核苷酸多态性与慢性阻塞性肺疾病(COPD)的相关性。方法:采用引物序列特异性聚合酶链反应—限制性片段长度多态性(PCR-RFLP)方法,分别对内蒙古地区184名蒙古族COPD病人和203名蒙古族健康对照组的ADAM33基因的Q-1、T+1、T 2、T 1、S 1五个位点的单核苷酸多态性进行检测,观察两组之间基因型和等位基因频率的差异。结果:ADAM33基因的4个SNPs与COPD相关(Q-1,P<0.001;T+1,P=0.020;T 2,P=0.018;S 1,P<0.001)。结论:ADAM33基因的Q-1、T+1、T 2、S 1位点与内蒙古地区蒙古族COPD具有相关性。

关键词：解整连蛋白和金属蛋白33 单核苷酸多态性慢性阻塞性肺疾病蒙古族 a disintegrin and metalloproteinase 33