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A common functional polymorphism (C→A substitution at position-863) in the promoter region of the tumour necrosis factor-α (TNF-α) gene associated with reduced circulating levels of TNF-α

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HUMAN MOLECULAR GENETICS 1999年第8期8卷 1443-1449页

作者： Skoog, T van't Hooft, FM Kallin, B Jovinge, S Boquist, S Nilsson, J Eriksson, P Hamsten, A Karolinska Inst Karolinska Hosp King Gustaf V Res Inst Atherosclerosis Res Unit S-17176 Stockholm Sweden Univ Lund Malmo Univ Hosp Dept Med S-21401 Malmo Sweden

Tumour necrosis factor-alpha (TNF-alpha) plays a key role in orchestrating the complex events involved in inflammation and immunity, Accordingly, TNF-alpha has been implicated in a wide range of autoimmune and infectious diseases, but also in conditions such as obesity and insulin resistance. The regulation of TNF-alpha expression in man is indicated to be partly genetically determined. We therefore screened a 1263 bp section of the proximal promoter of the TNF-alpha gene for common genetic variants affecting the transcriptional activity of the gene. Here we report the characterization of a common functional polymorphism in the promoter region of the TNF-alpha gene, a C-->A substitution at position -863, Electromobility shift assays provided evidence for a distinct difference in the binding of monocytic and hepatic nuclear factors to the -863C and -863A alleles, The rare -863A allele was associated with 31% lower transcriptional activity (P < 0.001) in chloramphenicol acetyltransferase (CAT) reporter gene studies in human hepatoblastoma (HepG2) cells, indicating that the -863C/A polymorphism influences the basal rate of transcription of the TNF-alpha gene in vitro, Allele frequencies were 0.83/0.17 amongst 254 apparently healthy men of Swedish origin, aged 35-50 years. In 156 men, the -863C/A polymorphism was associated with the serum TNF-alpha concentration, carriers of the rare A allele having a significantly lower TNF-alpha level (P < 0.05). It is concluded that the common -863C/A polymorphism in the promoter region of the TNF-alpha gene is functional in vitro in monocytic and hepatic cells and influences the serum TNF-alpha concentration in vivo in healthy middle-aged men.

关键词：等位基因结合部位/遗传学基因表达调控基因频率基因型连锁不平衡单核细胞激活素/血液单核细胞激活素/遗传学核蛋白质类/代谢点突变多态现象遗传蛋白质结合转录遗传/遗传学肿瘤细胞培养的肿瘤坏死因子α/遗传学成年人人类男(雄)性中年人

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Chemokine expression during acute rejection of rat kidneys

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SCANDINAVIAN JOURNAL OF IMMUNOLOGY 2000年第5期51卷 435-440页

作者： Grau, V Gemsa, D Steiniger, B Garn, H Univ Marburg Inst Anat & Cell Biol D-35033 Marburg Germany Univ Marburg Inst Immunol D-35033 Marburg Germany

During acute rejection of fully allogeneic rat renal allografts, few neutrophil granulocytes are detected, whereas an abundant infiltrate of macrophages and T lymphocytes becomes apparent. The mechanisms leading to this specific pattern of infiltration are not understood. We performed a sequential daily Northern blot analysis of the mRNA expression of the CC-chemokines MCP-1, MIP-1 alpha and RANTES and of the CXC-chemokines GRO/KC and MIP-2 in rat renal isografts (LEW --> LEW, n = 1 per day) and allografts during acute rejection (DA --> LEW, n = 3 per day). MCP-1 gene expression strongly increased on days 3-4 after allotransplantation and returned to control levels on day 6. The expression of MIP-1 alpha and RANTES continuously rose until day 3-4 and remained stable thereafter. Isografts displayed minor changes in CC-chemokine expression. In contrast to CC-chemokines, GRO/KC was expressed in low amounts during rejection and MIP-2 mRNA remained undetectable. In conclusion, the expression of the CC-chemokines MCP-1, MIP-1 and RANTES was clearly upregulated during rejection, whereas the mRNA of the CXC-chemokines MIP-2 and GRO/KC was not detected at all or remained at low levels. This pattern of chemokine gene expression is in good accordance with the predominant mononuclear leukocyte infiltrate in allografts.

关键词：趋化因子CCL2/遗传学趋化因子CCL3 趋化因子CCL4 趋化因子CCL5/遗传学趋化因子CXCL1 趋化因子CXCL2 趋化因子 CXC 趋化因子类/遗传学基因表达移植物排斥/免疫学生长物质/遗传学胞间信号肽类和蛋白质类肾移植/免疫学巨噬细胞炎性蛋白质类/遗传学单核细胞激活素/遗传学中性白细胞浸润/免疫学大鼠近交Lew 动物男(雄)性大鼠

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Antioxidant and inflammatory response after acute nitrogen dioxide and ozone exposures in C57Bl/6 mice

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INHALATION TOXICOLOGY 2000年第3期12卷 187-203页

作者： Johnston, CJ Reed, CK Avissar, NE Gelein, R Finkelstein, JN Univ Rochester Dept Environm Med Rochester NY 14642 USA Univ Rochester Dept Pediat Neonatol Rochester NY 14642 USA Univ Rochester Dept Surg Rochester NY 14642 USA

Ozone (O-3) and nitrogen dioxide (NO2) are highly reactive and toxic oxidant pollutants. The objective of this study is to compare chemokine, cytokine, and antioxidant changes elicited by acute exposures of O-3 and NO2 in a genetically sensitive mouse. Eight-week-old C57BI/6J mice were exposed to 1 or 2.5 ppm ozone or 15 of 30 ppm NO2 for 4 or 24 h. Changes in mRNA abundance in lung were assayed by slot blot and ribonuclease protection assay (RPA). Messages encoding metallothionein (Mt), heme oxygenase 1 (HO-1), and inducible nitric oxide synthase (iNOS) demonstrated increased message abundance after 4 and 24 h of exposure to either O-3 or NO2. Furthermore, increases in message abundance were of a similar magnitude for O-3 and NO2. Messages encoding eotaxin, macrophage inflammatory protein (MIP)-1 alpha, and MIP-2 were elevated after 4 and 24 h of exposure to I ppm ozone. Interleukin-6 was elevated after 4 h of exposure to ozone. After 4 h of 2.5 ppm ozone exposure, increased mRNAs of eotaxin, MIP-1 alpha: MIP-2, Mt, MO-1, and iNOS were elevated to a higher magnitude than were detected after I ppm ozone. Monocyte chemoattractant protein (MCP-1) was elevated following 15 ppm NO2 exposure. After 4 h of 30 ppm NO2 exposure, messages encoding eotaxin, MIP-1 alpha MIP-2, and MCP-I were elevated to levels similar to those detected after ozone exposure. Our results demonstrate a similar antioxidant and chemokine response during both O-3 and NO2 exposure. Induction of these messages is associated with the duration and concentration of exposure. These studies suggest that these gases exert toxic action through a similar mechanism.

关键词：投药吸入空气污染物/毒性趋化因子CCL2/遗传学趋化因子CCL2/代谢炎症趋化因子类/遗传学炎症趋化因子类/代谢趋化因子 CC 细胞因子类/遗传学细胞因子类/代谢血红素氧化酶(脱环)/遗传学血红素氧化酶(脱环)/代谢白细胞介素6/遗传学白细胞介素6/代谢肺/药物作用肺/代谢肺疾病间质性/化学诱导肺疾病间质性/代谢金属硫蛋白/遗传学金属硫蛋白/代谢小鼠近交C57BL 单核细胞激活素/遗传学单核细胞激活素/代谢一氧化氮合酶/遗传学一氧化氮合酶/代谢一氧化氮合酶Ⅱ型二氧化氮/投药和剂量二氧化氮/毒性核酸酶保护测定氧化剂光化学/投药和剂量氧化剂光化学/毒性臭氧/投药和剂量臭氧/毒性 RNA 信使/分析 RNA 信使/代谢动物男(雄)性小鼠

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Expression and regulation of macrophage inflammatory protein-2 gene by vanadium in mouse macrophages

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INFLAMMATION 2000年第2期24卷 127-139页

作者： Chong, IW Lin, SR Hwang, JJ Huang, MS Wang, TH Tsai, MS Hou, JJ Paulauskis, JD Kaohsiung Med Univ Dept Internal Med Kaohsiung 807 Taiwan Harvard Univ Sch Publ Hlth Dept Environm Hlth Boston MA 02115 USA

Environmental and occupational exposure to vanadium Oil dusts results in inflammation mainly confined to the respiratory tract. Macrophages apparently play an important role in mediating the inflammation via the production of many chemokines. In the current study, we investigated whether vanadium can regulate the gene expression of a CXC chemokine macrophage inflammatory protein-2 (MIP-2), and to determine the molecular mechanisms controlling MIP-2 gene expression. A mouse macrophage cell line RAW 264.7 was treated with sodium metavanadate (NaVO3) at the dose of 0.5, 5, or 10 mu g/ml V. Northern blot analysis showed that induction of MIP-2 mRNA expression was in a dose-dependent manner. To define the time course of the inflammatory response, RAW 264.7 cells were exposed to 5 mu g/ml V, MIP-2 mRNA in macrophages increased markedly as early as 1 h after treatment, maximally induced at 4 h and reduced to 2-fold above control levels by 6 and 8 h. The protein Levels of MIP-2 in conditioned media, measured by enzyme-linked immunosorbent assay (ELISA), was well correlated with the levels of MIP-2 mRNA following all of the treatments in the study. In addition, the increase in MIP-2 mRNA expression by vanadium was attenuated by co-treatment with the antioxidant. N-acetylcysteine (NAC), at the doses of 10 and 20 mM, suggesting that the induction of MIP-2 mRNA is mediated via the generation of reactive oxygen species (ROS). To further investigate transcriptional regulation of the MIP-2 gene expression by vanadium, we performed RNA decay assay by measuring the half-life of MIP-2 mRNA. Go-treatment of macrophages with the transcriptional inhibitor actinomycin D at 5 mu g/ml following exposure to 5 mu g/ml V for 4 h revealed complete stabilization of vanadium-induced MIP-2 mRNA and no sign of mRNA degradation, at least, for 6 h, in comparison to the half-life of MIP-2 mRNA was approximately 2.5 h by bacterial lipopolysaccharide (LPS) treatment, supporting post-transcriptional sta

关键词：乙酰半胱氨酸/药理学剂量效应关系药物酶联免疫吸附测定自由基清除剂/药理学基因表达/药物作用基因表达调控/药物作用巨噬细胞/化学单核细胞激活素/遗传学单核细胞激活素/分泌 RNA稳定性/药物作用 RNA 信使/生物合成 RNA 信使/药物作用转录遗传肿瘤细胞培养的钒酸盐类/药理学钒/药理学动物小鼠

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