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Reversibility of endurance training-induced changes on glucocorticoid sensitivity of monocytes by an acute exercise

CLINICAL ENDOCRINOLOGY 1999年第6期51卷 749-756页

作者： Duclos, M Minkhar, M Sarrieau, A Bonnemaison, D Manier, G Mormede, P Univ Bordeaux 2 Lab Neurogenet & Stress INSERM U471 Inst Francois Magendie F-33077 Bordeaux France Univ Bordeaux 2 Lab Physiol Exercise Musculaire & Sport F-33076 Bordeaux France Univ Bordeaux 2 Lab Immunol Mol F-33076 Bordeaux France

OBJECTIVE The aim of this study was to address the effect of endurance training on monocyte glucocorticoid sensitivity in vitro. METHODS For this purpose, in vitro dexamethasone inhibition of lipopolysaccharide (LPS)-induced interleukin-g (IL-6) secretion in cultures of peripheral monocytes was compared in 6 untrained subjects (UT) and in 6 endurance-trained (ET) men at 0800 h, 24h after the end of the last session of exercise (ET men). Moreover, to test the plasticity of these monocytes glucocorticoid sensitivity in ET men, the effect of an acute bout of exercise was further studied 2 h after the end of a 2-h run at 65-75% VO2max (1200 h) and compared to the results of UT after 4h of rest. RESULTS At 0800 h, monocytes from ET were more sensitive to LPS: lower LPS concentration in ET compared to UT men (0.003 vs. 0.03 mu g/ml) induced similar IL-6 concentrations in both ET and UT men (168.4 +/- 29.9 pg/ml with 0.003 mu g/ml LPS vs. 160.1 +/- 34.4 pg/ml with 0.03 mu g/ml LPS, ET vs. UT, respectively, P <0.05 for IL-6). No effect of sampling time was observed in UT subjects (0800 h vs. 1200 h), This was not the case for ET as at 1200 h, compared to preexercise values, the LPS-induced IL-6 production was not significantly different from that obtained in UT. Moreover, when sensitivity to dexamethasone (Dex) was studied and expressed as the percent inhibition of stimulated IL-6 production with 0.3 pg/ml LPS, at 0800 h the percent inhibition was lower in ET subjects compared to UT (P <0.01 ET vs. UT men) for each Dex concentration used [10(-11)-10(-8) M]. After exercise, the inhibitory effect of Dex on LPS-induced IL-6 production was restored in ET and was no longer significantly different from that obtained in UT. CONCLUSION We demonstrate in vitro plasticity of monocyte glucocorticoid sensitivity of endurance trained men, with training-induced decreased glucocorticoid sensitivity and acute exercise-induced return to the levels of the control untrained men.

关键词：方差分析血糖/分析病例对照研究细胞培养的地塞米松/药理学剂量效应关系药物运动(Exercise)/生理学糖皮质激素类/药理学氢化可的松/血液白细胞介素6/代谢脂多糖类/药理学单核细胞/药物作用单核细胞/代谢身体耐力/生理学刺激化学性成年人人类男(雄)性

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Amino-terminally modified RANTES analogues demonstrate differential effects on RANTES receptors

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第45期274卷 32478-32485页

作者： Proudfoot, AEI Buser, R Borlat, F Alouani, S Soler, D Offord, RE Schröder, JM Power, CA Wells, TNC Serono Pharmaceut Res Inst Geneva Switzerland LeukoSite Inc Cambridge MA 02142 USA Univ Kiel Dept Dermatol & Allergol Kiel Germany Ctr Med Univ Geneva Dept Biochim Med CH-1228 Geneva Switzerland

Modification of the amino terminus of regulated on activated normal T-cell expressed (RANTES) has been shown to have a significant effect on biological activity and produces proteins with antagonist properties. Two amino-terminally modified RANTES proteins, Met-RANTES and aminooxypentane-RANTES (AOP-RANTES), exhibit differential inhibitory properties on both monocyte and eosinophil chemotaxis, We have investigated their binding properties as well as their ability to activate the RANTES receptors CCR1, CCR3, and CCR5 in cell lines overexpressing these receptors, We show that Met-RANTES has weak activity in eliciting a calcium response in Chinese hamster ovary cells expressing CCR1, CCR3, and CCR5, whereas AOP-RANTES has full agonist activity on CCR5 but is less effective on CCR3 and CCR1, Their ability to induce chemotaxis of the murine pre-B lymphoma cell line, L1.2, transfected with the same receptors, consolidates these results, Monocytes have detectable mRNA for CCR1, CCR2, CCR3, CCR4, and CCR5, and they respond to the ligands for these receptors in chemotaxis but not always in calcium mobilization, AOP-RANTES does not induce calcium mobilization in circulating monocytes but is able to do so as these cells acquire the macrophage phenotype, which coincides with a concomitant up-regulation of CCR5, We have also tested the ability of both modified proteins to induce chemotaxis of freshly isolated monocytes and eosinophils, Cells from most donors do not respond, but occasionally cells from a particular donor do respond, particularly to AOP-RANTES, We therefore hypothesize that the occasional activity of AOP-RANTES to induce leukocyte chemotaxis is due to donor to donor variation of receptor expression.

关键词：抗HIV药/药理学结合竞争性趋化因子CCL5/类似物和衍生物趋化因子CCL5/药理学趋化作用/药物作用仓鼠亚科减量调节 HIV-1/致病力单核细胞/药物作用单核细胞/代谢受体 CCR1 受体 CCR3 受体 CCR5/代谢受体趋化因子/药物作用受体趋化因子/代谢表面特性动物

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Activation of primary human monocytes by the oxidized form of α1-antitrypsin

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第11期275卷 7693-7700页

作者： Moraga, F Janciauskiene, S Malmo Univ Hosp Dept Med Gastroenterol Hepatol Sect S-20502 Malmo Sweden

The oxidation of methionine residues in many proteins, including the serine proteinase inhibitor alpha 1-antitrypsin (AAT), can result in functional inactivation. In this study we investigated the pro-inflammatory properties of oxidized AAT (oxAAT), specifically its ability to activate human monocytes in culture. Monocytes stimulated with oxAAT at concentrations up to 0.2 mg/ml for 24 h showed significant elevation in monocyte tractant;tractant protein-1, cytokine interleukin-6, and tumor necrosis factor-a expression and increased NADPH oxidase activity. Monocytes activated with oxAAT showed surprising effects on lipid metabolism. Expression of low density lipoprotein (LDL) receptors increased by up to 76% compared with controls but was not accompanied by any changes in I-125-labeled LDL binding and, paradoxically, decreased LDL uptake, degradation, and intracellular cholesterol synthesis. oxAAT also down-regulated the scavenger receptor CD36, which takes up and is up-regulated by oxidized LDL and is down-regulated by cholesterol efflux, As a by-product of oxidative events accompanying inflammation, oxAAT has multiple effects on cytokine expression, generation of reactive oxygen species,and on intracellular lipid metabolism. The up-regulation of monocyte-derived reactive oxygen by oxAAT could potentially result in self-amplification of AAT oxidation and, thereby, the other effects deriving from it. This implies that there are as yet unidentified regulatory processes that control this cycle.

关键词：趋化因子CCL2/生物合成胆固醇/生物合成减量调节酶激活炎症介导素类/代谢白细胞介素6/生物合成脂蛋白类 LDL/代谢膜蛋白质类单核细胞/药物作用氧化还原受体免疫/生物合成受体 LDL/生物合成受体脂蛋白受体清道夫清道夫受体 B类肿瘤坏死因子α/生物合成 α1抗胰蛋白酶/化学 α1抗胰蛋白酶/药理学人类

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A novel proteolytic cleavage involved in Notch signaling:: The role of the disintegrin-metalloprotease TACE

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MOLECULAR CELL 2000年第2期5卷 207-216页

作者： Brou, C Logeat, F Gupta, N Bessia, C LeBail, O Doedens, JR Cumano, A Roux, P Black, RA Israël, A Inst Pasteur CNRS URA 1773 Unite Biol Mol Express Gen F-75724 Paris 15 France Inst Pasteur CNRS URA 1961 Unite Dev Lymphocytes F-75724 Paris 15 France Inst Pasteur CNRS URA 1773 F-75724 Paris 15 France Immunex Corp Dept Prot Chem Seattle WA 98101 USA

The Notch1 receptor is presented at the cell membrane as a heterodimer after constitutive processing by a furin-like convertase. Ligand binding induces the proteolytic release of Notch intracellular domain by a gamma-secretase-like activity. This domain translocates to the nucleus and interacts with the DNA-binding protein CSL, resulting in transcriptional activation of target genes. Here we show that an additional processing event occurs in the extracellular part of the receptor, preceding cleavage by the gamma-secretase-like activity. Purification of the activity accounting for this cleavage in vitro shows that it is due to TACE (TNF alpha-converting enzyme), a member of the ADAM (a disintegrin and metalloprotease domain) family of metalloproteases. Furthermore, experiments carried out on TACE(-/-) bone marrow-derived monocytic precursor cells suggest that this metalloprotease plays a prominent role in the activation of the Notch pathway.

关键词： ADAM蛋白质类氨基酸序列骨髓细胞/细胞学骨髓细胞/药物作用钙结合蛋白质类细胞分化分解素类/代谢胞间信号肽类和蛋白质类膜蛋白质类/代谢金属内肽酶类/代谢分子序列数据单核细胞/细胞学单核细胞/药物作用蛋白质生物合成蛋白质加工转译后蛋白质类受体 Notch1 受体细胞表面/代谢信号传导十四酰佛波乙酯/药理学转录因子动物小鼠

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Reactive oxygen intermediate-dependent NF-κB activation by interleukin-1β requires 5-lipoxygenase or NADPH oxidase activity

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MOLECULAR AND CELLULAR BIOLOGY 1999年第3期19卷 1950-1960页

作者： Bonizzi, G Piette, J Schoonbroodt, S Greimers, R Havard, L Merville, MP Bours, V Univ Liege Lab Med Chem Med Oncol B-4000 Liege Belgium Univ Liege Lab Fundamental Virol B-4000 Liege Belgium Univ Liege Pathol Lab B-4000 Liege Belgium

We previously reported that the role of reactive oxygen intermediates (ROIs) in NF-kappa B activation by proinflammatory cytokines was cell specific. However, the sources for ROIs in various cell types are Set to be determined and might include 5-lipoxygenase (5-LOX) and NADPH oxidase. 5-LOX and 5-LOX activating protein (FLAP) are coexpressed in lymphoid cells but not in monocytic or epithelial cells. Stimulation of lymphoid cells with interleukin-1 beta (IL-1 beta) led to ROI production and NF-kappa B activation, which could both be blocked by antioxidants or FLAP inhibitors, confirming that 5-LOX was the source of ROIs and was required for NF-kappa B activation in these cells. IL-1 alpha stimulation of epithelial cells did not generate any ROIs and NF-kappa B induction was not influenced by 5-LOX inhibitors. However, reintroduction of a functional 5-LOX system in these cells allowed ROI production and 5-LOX-dependent NF-kappa B activation. In monocytic cells, IL-1 beta treatment led to a production of ROIs which is independent of the 5-LOX enzyme but requires the NADPH oxidase activity. This pathway involves the Rad and Cdc42 GTPases, two enzymes which are not required for NF-kappa B activation by IL-1 beta in epithelial cells. In conclusion, three different cell-specific pathways lead to NP-kappa B activation by IL-I beta: a pathway dependent on ROI production by 5-LOX in lymphoid cells, an ROI- and 5-LOX-independent pathway in epithelial cells, and a pathway requiring ROI production by NADPH oxidase in monocytic tells.

关键词： 5-脂氧合酶活化蛋白类腺癌花生四烯酸盐5-脂氧合酶/生物合成载体蛋白质类/生物合成细胞周期蛋白质类/代谢 GTP磷酸水解酶类/代谢 GTP结合蛋白质类/代谢 HL-60细胞 HT29细胞白细胞介素1/代谢白细胞介素1/药理学 Jurkat细胞膜蛋白质类/生物合成单核细胞/药物作用单核细胞/代谢 NF-κB/代谢活性氧/代谢信号传导肿瘤细胞培养的 U937细胞 cdc42GTP结合蛋白质 racGTP结合蛋白质类 ρAGTP结合蛋白质人类

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A role for oxidative stress in suppressing serum immunoglobulin levels in lead-exposed Fisher 344 rats

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ARCHIVES OF ENVIRONMENTAL CONTAMINATION AND TOXICOLOGY 2000年第2期39卷 251-256页

作者： Ercal, N Neal, R Treeratphan, P Lutz, PM Hammond, TC Dennery, PA Spitz, DR Univ Missouri Dept Chem Rolla MO 65409 USA Univ Missouri Dept Biol Sci Rolla MO 65409 USA Sch Med Dept Pediat Stanford CA 94304 USA Washington Univ Mallinckrodt Inst Radiol Sect Canc Biol St Louis MO 63108 USA

Evidence implicating oxidative stress in toxicity during lead intoxication in vivo has opened new avenues for investigation of the mechanisms of lead-induced immunosuppression. The current study explores the possibility that lead-induced oxidative stress contributes to the immunosuppression observed during lead poisoning. Fisher 344 rats were exposed to 2,000 ppm lead acetate in their drinking water for 5 weeks. One week following removal of lead from the drinking water, significant reductions in serum levels of IgA, IgM, and IgG were detected. Significant increases in oxidative damage, based on malondialdehyde (MDA) content, were observed in peripheral blood mononuclear cells (PMCs) collected during the same experiments. In addition, MDA content increased in livers from lead-exposed rats. Following 5 weeks of lead exposure, administration of either 5.5 mmol/kg N-acetylcysteine (NAC) or 1 mmol/kg meso-2,3-dimercaptosuccinic acid (DMSA) in the drinking water for 1 week significantly reversed the inhibitory effects of lead on serum immunoglobulin (Ig) levels. Also, all parameters indicative of oxidative stress returned to control levels. These results suggest that oxidative stress contributes to suppressed serum Ig levels during lead intoxication in vivo, and that intervention with either a thiol antioxidant (NAC) or a metal chelator (DMSA) will alleviate this lead-induced suppression by correcting the prooxidant/antioxidant imbalance caused by lead exposure.

关键词：抗体生成/药物作用体重/药物作用过氧化氢酶/代谢色谱法高压液相免疫扩散免疫球蛋白类/血液免疫球蛋白类/药物作用免疫抑制法免疫抑制剂/毒性铅/代谢铅/毒性铅中毒/免疫学脂质过氧化作用/药物作用肝/药物作用肝/代谢丙二醛/代谢单核细胞/药物作用单核细胞/代谢氧化性应激/生理学大鼠近交F344 动物男(雄)性大鼠

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O⁶-benzylguanine enhances the in vitro immunotoxic activity of temozolomide on natural or antigen-dependent immunity

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 1999年第3期291卷 1292-1300页

作者： Alvino, E Pepponi, R Pagani, E Lacal, PM Nunziata, C Bonmassar, E D'Atri, S IDI IRCCS I-00167 Rome Italy Natl Res Council Inst Expt Med Rome Italy

Temozolomide (TMZ) is a new cytotoxic triazene compound of clinical interest that is able to generate methyl adducts at the O-6-guanine of DNA, which can be repaired by O-6-alkylguanine-DNA alkyltransferase (OGAT). It was previously found that triazene compounds are highly immunosuppressive in mice. In the present study, we investigate whether TMZ could affect immune functions of human competent cells and whether methylation of O-6-guanine could be involved in the immunosuppressive activity of the drug. Mononuclear cells (MNCs) obtained from peripheral blood of healthy donors were tested for OGAT activity and treated with TMZ alone or combined with the OGAT inhibitor O-6-benzylguanine. Control or drug-treated MNCs were then assayed for natural killer activity and for the ability to proliferate and to generate cytotoxic effector cells in response to interleukin-2 or allogeneic MT-2 tumor cells. The results show that TMZ inhibited both proliferation and induction of lytic activity in response to interleukin-2 or allogeneic MT-2 cells. Moreover, an inverse correlation was found between the OGAT activity of MNCs and their sensitivity to TMZ. The involvement of O-6-guanine methylation in the immunosuppressive effects of TMZ was further confirmed by the finding that O-6-benzylguanine increased the activity of the drug. On the other hand, the natural killer activity of MNCs was only moderately affected by TMZ, and no relationship was observed between OGAT levels and sensitivity to the drug. These data suggest that in patients with tumors who are undergoing TMZ treatment, the drug may impair immune responses involving cell proliferation, depending on OGAT levels of MNCs, and that O-6-benzylguanine may potentiate this activity.

关键词：抗体依赖细胞细胞毒性/药物作用抗肿瘤药烷基化/毒性细胞系达卡巴嗪/类似物和衍生物达卡巴嗪/毒性酶抑制剂/药理学鸟嘌呤/类似物和衍生物鸟嘌呤/药理学免疫细胞/药物作用免疫天然/药物作用免疫抑制剂/毒性白细胞介素2/药理学单核细胞/药物作用单核细胞/免疫学 T淋巴细胞调节性/药物作用 T淋巴细胞调节性/免疫学肿瘤细胞培养的人类

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Ability of Ni-containing biomedical alloys to activate monocytes and endothelial cells in vitro

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JOURNAL OF BIOMEDICAL MATERIALS RESEARCH 1999年第3期45卷 251-257页

作者： Wataha, JC Lockwood, PE Marek, M Ghazi, M Med Coll Georgia Sch Dent Dept Oral Rehabil Augusta GA 30912 USA Georgia Inst Technol Atlanta GA 30332 USA Georgia State Univ Atlanta GA 30303 USA

Nickel-containing alloys commonly are used in medical and dental applications that place them into longterm contact with soft: tissues. The release of Ni ions from these alloys is disturbing because of the toxic, immunologic, and carcinogenic effects that have been documented for some Ni compounds. In particular, Ni ions in solution recently have been shown to cause expression of inflammatory mediators, such as interleukin-1 beta (IL-1 beta), tumor necrosis factor-alpha (TNF-alpha), and intercellular adhesion molecules (ICAMs) from keratinocytes, monocytes, and endothelial cells. However, the ability of the solid alloys themselves to induce these inflammatory effects has not been demonstrated. An in vitro system was used to determine if Ni-containing biomedical alloys could cause secretion of either IL-1 beta or TNF-alpha from monocytes or expression of ICAMs on endothelial cells. Pure nickel, titanium, and three biomedical alloys-18-8 stainless steel, NiTi, and Rexillium III-were evaluated. First, it was determined whether or not the alloys or pure metals could cause cytotoxicity to THP-1 human monocytes or human microvascular endothelial cells (HMVECs) by measuring the succinic dehydrogenase (SDH) activity of the cells. Then, using identical conditions of exposure, the secretion of IL-1 beta or TNP-alpha from monocytes or ICAM-1 expression on the HMVECs was determined. Only pure nickel suppressed (by 48% compared to Teflon controls) the SDH activity of the HMVECs or THT-1 monocytes. No alloy or metal caused the HMVECs to express ICAM-1, but the NiTi alloy caused a significant (ANOVA/Tukey) secretion of IL-1 beta from the THP-1 monocytes. Secretion of TNF-alpha induced by NiTi was detectable but not statistically significant. The levels of IL-1 beta secretion from monocytes were sufficient to induce ICAM-1 expression on HMVECs. The release of Ni from the NiTi was a logical suspect in causing the IL-1 beta secretion by monocytes, but its role was not confirmed since

关键词：合金/毒性毛细血管/细胞学毛细血管/药物作用细胞存活/药物作用细胞培养的内皮血管/细胞学内皮血管/药物作用内皮血管/代谢胞间黏附分子1/生物合成白细胞介素1/代谢巨噬细胞活化/药物作用单核细胞/化学单核细胞/药物作用镍/分析镍/毒性琥珀酸脱氢酶/代谢钛/毒性肿瘤坏死因子α/代谢人类

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Evaluation of a human monocytic cell line THP-1 model for assay of the intracellular activities of antimicrobial agents against Legionella pneumophila

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JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY 2000年第4期46卷 589-594页

作者： Takemura, H Yamamoto, H Kunishima, H Ikejima, H Hara, T Kanemitsu, K Terakubo, S Shoji, Y Kaku, M Shimada, J St Marianna Univ Dept Microbiol Sch Med Miyamae Ku Kawasaki Kanagawa 2168511 Japan

We examined the intracellular activities of 11 antimicrobial agents against Legionella pneomophila using a human monocyte-derived cell line, THP-1. Colony counting and microscopic examination of L. pneumophila co-incubated with THP-1 cells (5 x 10(5) cells/well) were performed. Both extra- and intra-cellular multiplication of L. pneumophila were observed and were dependent on the inoculum of L. pneumophila in the culture;L. pneumophila did not grow in the cell culture medium alone. Light microscopic examination confirmed that extracellular L. pneumophila originated from THP-l cells disrupted by bacterial multiplication. L. pneumophila multiplied by 3-4 logs after 24 h incubation with THP-1 cells and their number remained stable at 10(6)-10(7) cfu/mL until 72 h. The results of viability studies using four antimicrobial agents-ciprofloxacin, erythromycin, minocycline and rifampicin-demonstrated that our system was suitable for the intracellular activity assay. We used a concept of 'minimum extracellular concentration inhibiting intracellular multiplication' (MIEC) to evaluate the intracellular activity of antimicrobial agents. The MIECs of three beta -lactams were markedly higher than their conventional MICs while those of macrolides, quinolones, rifampicin and minocycline were similar to their MICs. Our results suggest that evaluation of the clinical efficacy of drugs against L. pneumophila should include determination of their intracellular activity against the bacteria, which could be measured using our assay system in THP-1 cells.

关键词：抗菌药/药理学抗感染药/药理学抗生素类抗结核/药理学细胞系环丙沙星/药理学红霉素/药理学嗜肺军团病杆菌/药物作用微生物敏感性试验/方法米诺环素/药理学单核细胞/药物作用单核细胞/微生物学利福平/药理学人类

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ABCG1 (ABC8), the human homolog of the Drosophila white gene, is a regulator of macrophage cholesterol and phospholipid transport

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 2000年第2期97卷 817-822页

作者： Klucken, J Büchler, C Orsó, E Kaminski, WE Porsch-Özcürümez, M Liebisch, C Kapinsky, M Diederich, W Drobnik, W Dean, M Allikmets, R Schmitz, G Univ Regensburg Inst Clin Chem & Lab Med D-93042 Regensburg Germany NCI Lab Genome Divers Frederick MD 21702 USA Columbia Univ Dept Ophthalmol New York NY 10032 USA Columbia Univ Dept Pathol New York NY 10032 USA

Excessive uptake of atherogenic lipoproteins such as modified low-density lipoprotein complexes by vascular macrophages leads to foam cell formation, a critical step in atherogenesis, Cholesterol afflux mediated by high-density lipoproteins (HDL) constitutes a protective mechanism against macrophage lipid overloading. The molecular mechanisms underlying this reverse cholesterol transport process are currently not fully understood. To identify effector proteins that are involved in macrophage lipid uptake and release, we searched for genes that are regulated during lipid influx and efflux in human macrophages using a differential display approach. We report here that the ATP-binding cassette (ABC) transporter ABCG1 (ABC8) is induced in monocyte-derived macrophages during cholesterol influx mediated by acetylated low-density lipoprotein. Conversely, lipid efflux in cholesterol-laden macrophages, mediated by the cholesterol acceptor HDL3, suppresses the expression of ABCG1, Immunocytochemical and flow cytometric analyses revealed that ABCG1 is expressed on the cell surface and in intracellular compartments of cholesterol-laden macrophages. Inhibition of ABCG1 protein expression using an antisense strategy resulted in reduced HDL3-dependent efflux of cholesterol and choline-phospholipids. In a comprehensive analysis of the expression and regulation of all currently known human ABC transporters, we identified an additional set of ABC genes whose expression is regulated by cholesterol uptake or HDL3-mediated lipid release, suggesting a potential function for these transporters in macrophage lipid homeostasis. Our results demonstrating a regulator function for ABCG1 in cholesterol and phospholipid transport define a biologic activity for ABC transporters in macrophages.

关键词： ATP结合匣式转运子/分析 ATP结合匣式转运子/遗传学 ATP结合匣式转运子/生理学生物转运细胞培养的胆固醇/代谢果蝇蛋白质类眼蛋白质类/遗传学基因表达调控/药物作用免疫组织化学昆虫蛋白质类/遗传学动力学脂蛋白类 HDL/药理学脂蛋白类 LDL/药理学巨噬细胞/化学巨噬细胞/药物作用巨噬细胞/代谢单核细胞/化学单核细胞/药物作用单核细胞/代谢寡核苷酸类反义/药理学磷脂类/代谢 RNA 信使/遗传学 RNA 信使/代谢组织分布动物女(雌)性人类男(雄)性

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