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中华肿瘤防治杂志 2009年第17期16卷 1295-1297页

作者：丁新民徐勤枝周平坤冯华松段蕴铀中国人民解放军海军总医院呼吸内科北京100037 军事医学科学院放射与辐射医学研究所北京100850

目的:了解4-(甲基亚硝胺)-1-(3-吡啶)-1-丁酮〔4-(methyl-nitrosamino)-1-(3-py-ridyl)-1-butanone,NNK〕对支气管上皮细胞(BEP2D)端粒酶活性的影响。方法:NNK处理BEP2D细胞后,用四甲基偶氮唑蓝(MTT)检测细胞存活率,用端粒酶重复序列扩增-酶联免疫吸附法(TRAP-EL-ISA)检测端粒酶活性,蛋白质印迹法检测端粒酶催化亚单位人端粒酶逆转录酶(hTERT)蛋白的表达。结果:10mg/LNNK孵育24、48及72h后,BEP2D细胞存活率不受影响,但其端粒酶活性均增高,而hTERT蛋白表达增高则在孵育48及72h时间点。结论:NNK可刺激BEP2D细胞端粒酶活化及hTERT蛋白的表达。

关键词：支气管/细胞学细胞,培养的细胞转化,肿瘤亚硝胺类

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氯化镉诱发16HBE细胞恶性转化中hOGG1基因表达和序列变化的研究

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中华肿瘤防治杂志 2008年第3期15卷 161-164页

作者：周志衡雷毅雄王彩霞王敏魏莲纪卫东广州医学院公共卫生与全科医学学院广东广州510182 广州医学院附属市一医院血液科广东广州510180

目的:探讨氯化镉诱发人支气管上皮(16HBE)细胞系恶性转化过程中hOGG1基因mRNA和蛋白动态变化的规律及其序列变化情况。方法:用反转录-聚合酶链反应(PT-PCR)和免疫组织化学(SP法)检测16HBE细胞、氯化镉恶性转化16HBE细胞系不同阶段(第5... 详细信息

目的:探讨氯化镉诱发人支气管上皮(16HBE)细胞系恶性转化过程中hOGG1基因mRNA和蛋白动态变化的规律及其序列变化情况。方法:用反转录-聚合酶链反应(PT-PCR)和免疫组织化学(SP法)检测16HBE细胞、氯化镉恶性转化16HBE细胞系不同阶段(第5、15和35代细胞及成瘤细胞)hOGG1基因mRNA和蛋白的表达情况;用直接测序法分析hOGG1基因第7外显子的序列情况。结果:随着转化代数的增加,hOGG1基因mRNA和蛋白的表达逐渐降低,到第15代细胞后表达明显下降(P<0.05);hOGG1基因第7外显子第162位点插入一个腺嘌呤A,为移码突变。结论:hOGG1基因水平的下调和突变可能是氯化镉分子致癌的重要机制。

关键词：氯化镉支气管/细胞学基因突变

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体外构建气管黏膜上皮组织的研究

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第四军医大学学报 2008年第3期29卷 208-210页

作者：吴明明崔鹏程赵大庆郑德育段小红第四军医大学唐都医院耳鼻咽喉科陕西西安710038 第四军医大学基础部病理学教研室陕西西安710033

目的:应用组织工程原理和方法在体外构建气管黏膜上皮组织.方法:将原代兔气管上皮细胞种植在铺有鼠尾胶原的小肠黏膜下层(SIS)上培养,在体外构建气管黏膜上皮组织,培养1wk后行HE染色,对气管上皮细胞行免疫细胞学鉴定.结果:原代气管上皮... 详细信息

目的:应用组织工程原理和方法在体外构建气管黏膜上皮组织.方法:将原代兔气管上皮细胞种植在铺有鼠尾胶原的小肠黏膜下层(SIS)上培养,在体外构建气管黏膜上皮组织,培养1wk后行HE染色,对气管上皮细胞行免疫细胞学鉴定.结果:原代气管上皮细胞培养1wk后增殖旺盛,10d时上皮细胞分布范围更广.将构建的气管黏膜上皮组织行HE染色,显示有气管黏膜上皮和SIS双层结构.抗角蛋白单克隆抗体免疫细胞化学反应阳性显色率可达90%左右.结论:将铺有鼠尾胶原的SIS复合气管上皮细胞生长,成功的在体外构建出组织工程化的气管黏膜上皮组织.

关键词：支气管/细胞学上皮细胞小肠黏膜下层组织培养组织工程

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卷烟烟气凝集物诱发人支气管上皮细胞转化的初步研究

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安徽医科大学学报 2007年第3期42卷 265-268页

作者：徐国蕊郑红朱茂祥汪思应安徽医科大学基础医学院病理生理学教研室合肥230032 军事医学科学院放射医学研究所北京100850

目的建立卷烟烟气凝集物(CSC)诱发细胞转化的模型,模拟吸烟致肺癌的过程。方法利用CSC染毒体外培养的人支气管上皮细胞系BEP2D,诱导转化。结果以0·001支烟/ml剂量每代染毒24h,连续染毒30代共720h后,诱发细胞发生明显转化改变,细胞... 详细信息

目的建立卷烟烟气凝集物(CSC)诱发细胞转化的模型,模拟吸烟致肺癌的过程。方法利用CSC染毒体外培养的人支气管上皮细胞系BEP2D,诱导转化。结果以0·001支烟/ml剂量每代染毒24h,连续染毒30代共720h后,诱发细胞发生明显转化改变,细胞逐渐发生生长动力学和形态学的改变,生长失去接触抑制,获得对血清诱导末端分化的抗性和锚着独立性生长能力,与对照细胞比较均有统计学意义上的增强。结论从BEP2D到CSC转化的细胞能够在一定程度上模拟体内肿瘤的发生发展过程,可以为深入了解吸烟致肺癌发生多阶段过程中的细胞和分子机制提供研究模型。

关键词：亚硝胺类上皮细胞突变烟草/副作用烟雾/副作用支气管/细胞学

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Integrin αvβ8-mediated activation of transforming growth factor-β inhibits human airway epithelial proliferation in intact bronchial tissue

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AMERICAN JOURNAL OF PATHOLOGY 2003年第2期163卷 533-542页

作者： Fjellbirkeland, L Cambier, S Broaddus, VC Hill, A Brunetta, P Dolganov, G Jablons, D Nishimura, SL Univ Calif San Francisco San Francisco Gen Hosp Dept Anat Pathol San Francisco CA USA Univ Calif San Francisco San Francisco Gen Hosp Lung Biol Ctr San Francisco CA USA Univ Calif San Francisco Mt Zion Canc Ctr San Francisco CA 94143 USA Univ Calif San Francisco Dept Med San Francisco CA 94143 USA Univ Calif San Francisco Div Pulm San Francisco CA 94143 USA Univ Calif San Francisco Dept Surg San Francisco CA 94143 USA

Transforming growth factor (TGF)-beta is a potent multifunctional cytokine that is an essential regulator of epithelial proliferation. Because TGF-beta is expressed almost entirely in a latent state in vivo, a major source of regulation of TGF-beta function is its activation. A subset of integrins, alphavbeta8 and alphavbeta6, which are expressed in the human airway, has recently been shown to activate latent TGF-beta in vitro, suggesting a regulatory role for integrins in TGF-beta function in vivo. Here we have developed a novel, biologically relevant experimental model of human airway epithelium using intact human bronchial tissue. We have used this model to determine the function of integrin-mediated activation of TGF-beta in the airway. In human bronchial fragments cultured in vitro, authentic epithelial-stromal interactions were maintained and integrin and TGF-beta expression profiles correlated with profiles found in normal lung. In addition, in this model, we found that either the integrin alphavbeta8 or TGF-beta could inhibit airway epithelial cell proliferation. Furthermore, we found that one mechanism of integrin-alphavbeta8-dependent inhibition of cell proliferation was through activation of TGF-beta because anti-beta38 antibody blocked the majority (76%) of active TGF-beta released from bronchial fragments. These data provide compelling evidence for a functional role for integrinmediated activation of TGF-beta in control of human airway epithelial proliferation in vivo.

关键词：支气管/细胞学支气管/代谢细胞分裂/生理学培养技术基因表达谱内环境稳定整合素类/代谢角蛋白质类/代谢 Ki-67抗原/代谢呼吸道黏膜/细胞学呼吸道黏膜/代谢转化生长因子β/代谢老年人老年人 80以上女(雌)性人类男(雄)性中年人

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A histological and immunohistochemical study of the humoral immune system of the lungs in young thoroughbred horses

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JOURNAL OF COMPARATIVE PATHOLOGY 1999年第4期120卷 347-356页

作者： Blunden, AS Gower, SM Anim Hlth Trust Ctr Prevent Med Newmarket CB8 7UU Suffolk England

Lungs were obtained from 16 Thoroughbred horses, aged 1 day to 2 years, which had died or been humanely killed for reasons unrelated to disease of the lower respiratory tract. The lungs were then subjected to a histological and immunohistochemical examination of the humoral immune system. At birth there was no evidence of organized lymphoid tissue, and lymphocytes and plasma cells were virtually absent in all tissue compartments in the first week of life. However, by 12 weeks;foals exhibited well developed bronchus-and bronchiole-associated lymphoid tissue, but this had regressed progressively at and 2 years of age. Plasma cells were present in large numbers in the walls of bronchi and bronchioles in foals aged 8 to 12 weeks. IgA-producing plasma cells were common in the lower respiratory tract of these young horses, in addition to IgG- and Ig;IgM-producing plasma cells. (C) 1999 W.B. Saunders Company Limited.

关键词：衰老/免疫学动物新生抗体生成/免疫学支气管/细胞学马/免疫学免疫球蛋白A/代谢免疫球蛋白G/代谢免疫球蛋白M/代谢免疫组织化学肺/细胞学肺/免疫学肺/代谢淋巴组织/细胞学浆细胞/细胞学浆细胞/代谢动物女(雌)性男(雄)性

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Asbestos and cigarette smoke cause increased DNA strand breaks and necrosis in bronchiolar epithelial cells in vivo

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FREE RADICAL BIOLOGY AND MEDICINE 2000年第8期28卷 1295-1299页

作者： Jung, M Davis, WP Taatjes, DJ Churg, A Mossman, BT Univ Vermont Coll Med Dept Pathol Burlington VT 05405 USA Univ British Columbia Dept Pathol Vancouver BC Canada

Coexposures to asbestos and cigarette smoke cause increased risks of lung cancer in asbestos workers. Although these carcinogens cause DNA damage to epithelial cells in vitro via generation of reactive oxygen species (ROS), it is unclear whether they cause injury to bronchiolar epithelial cells (i.e., the target cells of lung cancers in vivo). We exposed rats to amosite asbestos, cigarette smoke, and the two agents in combination for 1, 2, and 14 d. Numbers of cells exhibiting DNA strand breaks in comparison to sham rats were then evaluated in lungs using the terminal deoxynucleotidyl transferase (TDT)-mediated dUTP-biotin nick end labeling (TUNEL) method and by transmission electron microscopy (TEM). Increases in TUNEL-positive, necrotic epithelial cells occurred after exposure to asbestos alone and in an additive fashion after smoke and asbestos in combination. These results indicate that DNA strand breakage and necrosis are prominent mechanisms of injury by asbestos fibers and cigarette smoke in vivo to epithelial cells of the respiratory tract, thus validating in vitro observations from a number of laboratories. (C) 2000 Elsevier Science Inc.

关键词：细胞凋亡/药物作用石棉铁/毒性支气管/细胞学支气管/药物作用辅致癌作用 DNA损伤药物协同作用上皮细胞/化学上皮细胞/药物作用原位缺口末端标记坏死植物有毒大鼠 Sprague-Dawley 活性氧烟/副作用烟草动物男(雄)性大鼠

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Induction of the cytochrome P450 gene CYP26 during mucous cell differentiation of normal human tracheobronchial epithelial cells

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MOLECULAR PHARMACOLOGY 2000年第3期58卷 483-490页

作者： Kim, SY Adachi, H Koo, JS Jetten, AM NIEHS Cell Biol Sect Pulm Pathobiol Lab NIH Res Triangle Pk NC 27709 USA

In this study, the expression of CYP26 is examined in relation to retinoid-induced mucosecretory differentiation in human tracheobronchial epithelial (HTBE) cells and compared with that in human lung carcinoma cell lines. In HTBE cells, retinoic acid (RA) inhibits squamous differentiation and induces mucous cell differentiation as indicated by the suppression of transglutaminase I and increased expression of the mucin gene MUC2. The latter is accompanied by increased expression of CYP26 mRNA. RA is required but not sufficient to induce RAR beta, CYP26, and MUC2 mRNA because induction is only observed in confluent but not in logarithmic cultures, suggesting that additional factors are critical in their regulation. CYP26 mRNA can be induced by the RAR-selective retinoid 4-(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-anthracenyl)-benzoic acid (TTAB) but not by the RXR-selective retinoid SR11217 or the anti-activator-protein 1-selective retinoid SR11302. RAR alpha-, beta-, and gamma-selective retinoids are able to induce CYP26;this induction is inhibited by the RAR alpha-selective antagonist Ro41-5253. TTAB is able to induce CYP26 mRNA expression in only a few of the lung carcinoma cell lines tested. The lack of CYP26 induction in many carcinoma cell lines may relate to previously reported defects in the retinoid-signaling pathway. The induction of CYP26 correlated with increased metabolism of RA into 18-hydroxy-, 4-oxo-, and 4-hydroxy-RA. The latter metabolite was shown to be able to induce MUC2 and MUC5AC expression in HTBE cells. Our results demonstrate that in normal HTBE cells, CYP26 expression is closely associated with mucous cell differentiation and that many lung carcinoma cells exhibit increased RA metabolism and a defective regulation of CYP26.

关键词：抗肿瘤药/代谢抗肿瘤药/药理学支气管/细胞学支气管/生理学细胞分化/药物作用细胞分化/遗传学细胞系细胞色素P450酶系统/生物合成细胞色素P450酶系统/遗传学上皮细胞/细胞学上皮细胞/生理学基因表达调控/药物作用肺肿瘤 RNA 信使/生物合成受体维甲酸/代谢维甲酸/类似物和衍生物维甲酸/代谢维甲酸/药理学肿瘤细胞培养的人类

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Reverse transcription-competitive multiplex PCR improves quantification of mRNA in clinical samples -: Application to the low abundance CFTR mRNA

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CLINICAL CHEMISTRY 1999年第5期45卷 619-624页

作者： Loitsch, SM Kippenberger, S Dauletbaev, N Wagner, TOF Bargon, J Univ Hosp Frankfurt Dept Internal Med Div Pulm Med D-60590 Frankfurt Germany Univ Hosp Frankfurt Dept Dermatol D-60590 Frankfurt Germany

Background: To monitor gene therapy, we wished to quantify cystic fibrosis transmembrane conductance regulator (CFTR) mRNA. We developed a PCR-based method to measure CFTR mRNA in clinical samples. Methods: Expression was determined by reverse transcription-competitive multiplex PCR (RCMP) for CFTR and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) transcripts, and for serial dilutions of two internal cDNA standards consisting of CFTR and GAPDH mutants containing short deletions. The RCMP used simultaneous amplification of the gene of interest with a reporter gene in one reaction tube. The expression of CFTR was calculated with reference to the amount of GAPDH to correct for variations in initial RNA loading. Results: Amplification of cDNAs derived from different amounts of RNA (1-4 mu g) gave similar GAPDH/CFTR ratios, with a coefficient of variation (CV) below 7.5%. RCMP was applied on nasal and bronchial brushings and shows a high variability of CFTR expression in non-cystic fibrosis donors. Conclusion: This method is precise and reproducible and advantageous for use with limited amounts of tissue, such as from biopsies or from nasal or bronchial brushings. (C) 1999 American Association for Clinical Chemistry.

关键词：支气管/化学支气管/细胞学细胞培养的囊性纤维化跨膜传导调节因子/分析囊性纤维化跨膜传导调节因子/遗传学电泳琼脂凝胶甘油醛-3-磷酸脱氢酶类/分析甘油醛-3-磷酸脱氢酶类/遗传学突变鼻/化学鼻/细胞学 RNA 信使/分析结果可重复性逆转录聚合酶链反应敏感性与特异性人类

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CD40 expression by human bronchial epithelial cells

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SCANDINAVIAN JOURNAL OF IMMUNOLOGY 1999年第4期49卷 355-361页

作者： Gormand, F Briere, F Peyrol, S Raccurt, M Durand, I Aït-Yahia, S Lebecque, S Banchereau, J Pacheco, Y Ctr Hosp Lyon Sud Lab Immunoallergol Resp F-69310 Pierre Benite France Schering Plough Lab Rech Dardilly France Inst Pasteur Lyon France Baylor Inst Dallas TX USA

CD40 is a 50-kDa protein expressed on B cells, dendritic cells, monocytes and epithelial cells, but the distribution of CD40 expression in humans is not completely known. It binds to a ligand (CD40 L) which is expressed essentially on activated T cells. The interaction between CD40 and CD40 L plays important roles in immune responses. CD40 expression was investigated on bronchial tissues and human bronchial cell lines using immunohistochemistry, immunofluorescence staining and analysis with a cytometer, respectively. Constitutive CD40 expression, but not that of CD40 L, was slightly detectable on normal human bronchial epithelial cells (HBEC) in situ and on an adult lung adenocarcinoma (SKLU1) cell line, while another cell line, a bronchial transformed SV40 cell line (WI26VA4), was negative for CD40. Among the various cytokines tested, only interferon (IFN)-gamma was found to induce CD40 expression on WI26VA4. Tumour necrosis factor (TNF)-alpha was the best cytokine able to up-regulate CD40 in SKLU1 cells. A combination of IFN-gamma and TNF-alpha was slightly more effective than the cytokine alone at up-regulating CD40 expression on both cell lines. We further investigated the functional consequences of CD40 ligation on both cell lines. These bronchial cells expressed CD40, HLADR and CD54 under basal conditions or when stimulated by cytokines. Stimulation through CD40 did not affect cell-surface-antigen expression on either cell line. The production of cytokines such as interleukin (IL)-6 and granulocyte macrophage-colony stimulating factor (GM-CSF) by HBEC has been described. SKLU1 and WI26VA4 cells released IL-6 and GM-CSF spontaneously. Whatever the case, CD40 engagement did not modulate spontaneous or TNF-alpha-induced production of these two cytokines. These data indicate fur the first time that normal HBEC express CD40 in situ. Further investigations are required in order to determine the role of CD40 on normal HBEC.

关键词：支气管/细胞学支气管/免疫学支气管/代谢细胞系细胞因子类/药理学上皮细胞/药物作用上皮细胞/免疫学上皮细胞/代谢肿瘤细胞培养的女(雌)性人类男(雄)性中年人

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