硫氧还蛋白结合蛋白2/维生素D上调蛋白1（VDUP1）在哮喘患者外周血嗜酸细胞的表达和功能研究
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摘要
研究背景
支气管哮喘是常见的慢性疾病，研究哮喘的分子病理机制是有效控制哮喘的前提。针对哮喘的遗传学基础、与环境因素的关系、免疫机制等研究证实哮喘是受遗传和环境因素影响的复杂的多基因疾病。同时也发现很多尚不明了和有争议的问题，其中关于嗜酸性粒细胞(EOS)的作用是最大的争论焦点之一。
EOS是参与哮喘病理过程的炎症细胞之一。目前已经证明哮喘中EOS作用过程如下：抗原递呈细胞将抗原递呈到细胞表面，导致Th2细胞分化并产生Th2细胞因子，其中IL-5、IL-13、GM-CSF促进骨髓CD34~+干细胞向EOS方向分化，在IL-5诱导下，细胞从骨髓向血管迁移；IL-4、IL-13诱导血管细胞粘附分子(VCAM-1)表达，结合到其在EOS表面受体(VLA-4)，使得血管内EOS利于穿过血管壁，到达Th2细胞介导的炎症反应部位；活化的EOS作用于气道壁多种细胞，或者分泌Th2细胞因子，导致气道粘膜以EOS浸润为特征的炎症、粘液分泌增加、气道高反应性、基底膜胶原沉积等哮喘病理生理过程。
而哮喘中EOS在活化、发挥炎症效应过程中细胞内部信号转导调节、分子调控机制以及这些细胞内部分子调控与细胞活化、发挥其在哮喘中病理作用的关系有待进一步探讨。我们实验室从哮喘发作过程中EOS基因差异表达入手，希望发现哮喘发作过程中EOS某些有意义的表达变化的基因，以及这些基因表
Background
As a common chronic disease, the incidence of asthma increase year after year. It is fundamental that investigate the molecular mechanism of asthma which including genetic factors, environment, immunity, the inflammation and reconstruction of bronchus for controlling asthma. It has been approved that asthma is a polygene disease influenced by genetic variants and environment. Some controversy exist in the mechanism of asthma, including the role of eosinophils(EOS) in asthma.
EOS is one of the effect cells in asthma. It has been proved that APC present antigen to surface of cell and result in the differentiation of Th2 that secrete cytokines, such as IL-4, IL-5 and IL-13. These cytokines facilitate CD34+ hematopoietic cell differentiate to EOS lineage in marrow. And then, the cells migrate from marrow to blood vessel induced by IL-5. VCAM-1, induced by IL-4 and IL-13 in endothelium, which band with receptor such as VLA-4 on the surface of EOS. So EOS can traverse vessel wall easily and recruit to the position of inflammation. The activated EOS act on all kinds of cells, such as fibroblast, muscle cells, epithelium, and secrete
支气管哮喘是常见的慢性疾病，研究哮喘的分子病理机制是有效控制哮喘的前提。针对哮喘的遗传学基础、与环境因素的关系、免疫机制等研究证实哮喘是受遗传和环境因素影响的复杂的多基因疾病。同时也发现很多尚不明了和有争议的问题，其中关于嗜酸性粒细胞(EOS)的作用是最大的争论焦点之一。
EOS是参与哮喘病理过程的炎症细胞之一。目前已经证明哮喘中EOS作用过程如下：抗原递呈细胞将抗原递呈到细胞表面，导致Th2细胞分化并产生Th2细胞因子，其中IL-5、IL-13、GM-CSF促进骨髓CD34~+干细胞向EOS方向分化，在IL-5诱导下，细胞从骨髓向血管迁移；IL-4、IL-13诱导血管细胞粘附分子(VCAM-1)表达，结合到其在EOS表面受体(VLA-4)，使得血管内EOS利于穿过血管壁，到达Th2细胞介导的炎症反应部位；活化的EOS作用于气道壁多种细胞，或者分泌Th2细胞因子，导致气道粘膜以EOS浸润为特征的炎症、粘液分泌增加、气道高反应性、基底膜胶原沉积等哮喘病理生理过程。
而哮喘中EOS在活化、发挥炎症效应过程中细胞内部信号转导调节、分子调控机制以及这些细胞内部分子调控与细胞活化、发挥其在哮喘中病理作用的关系有待进一步探讨。我们实验室从哮喘发作过程中EOS基因差异表达入手，希望发现哮喘发作过程中EOS某些有意义的表达变化的基因，以及这些基因表
Background
As a common chronic disease, the incidence of asthma increase year after year. It is fundamental that investigate the molecular mechanism of asthma which including genetic factors, environment, immunity, the inflammation and reconstruction of bronchus for controlling asthma. It has been approved that asthma is a polygene disease influenced by genetic variants and environment. Some controversy exist in the mechanism of asthma, including the role of eosinophils(EOS) in asthma.
EOS is one of the effect cells in asthma. It has been proved that APC present antigen to surface of cell and result in the differentiation of Th2 that secrete cytokines, such as IL-4, IL-5 and IL-13. These cytokines facilitate CD34+ hematopoietic cell differentiate to EOS lineage in marrow. And then, the cells migrate from marrow to blood vessel induced by IL-5. VCAM-1, induced by IL-4 and IL-13 in endothelium, which band with receptor such as VLA-4 on the surface of EOS. So EOS can traverse vessel wall easily and recruit to the position of inflammation. The activated EOS act on all kinds of cells, such as fibroblast, muscle cells, epithelium, and secrete
引文
[1] Caramori G, Papi A. Oxidant and asthma. Thorax 2004;59:170-173.
[2] Dworski R. Oxidant stress in asthma. Thorax 2000,55:51-53.
[3] Barnes PJ. Reactive oxygen species and airway inflammation. Free Redic Biol Med 1990;9:235-243.
[4] Barnes PJ, Chung KF, Page CP. Inflammatory mediators of asthma: on update. Pharmacol Rev 1998;50:515-596.
[5] Bowler RP, Crapo JD. Oxidative stress in allergic respiratory diseases. J Allergy Clin Immunol 2002;110:349-356.
[6] Dworski R. Oxidant stress in asthma. Thorax 2000;55(2):S51-S53.
[7] Henricks PA, Nijkamp FP. Reactive oxygen species as mediators in asthma. Pulm Pharmacol Ther 2001; 14:409-420.
[8] Rahman I, MacNee W. Reactive oxygen species. In: Barnes PJ, Drazen J, Rennard S,et al, eds. Asthma and COPD. London: Academic Press 2002:243-254.
[9] Aldridge RE, Chan T, van Dalen CJ, et al. Eosinophil peroxidase produces hypobromous acid in the airways of stable asthmatics. Free Radic Biol Med 2002;33:847-856.
[10] Ricciardolo FL. Multiple roles of nitric oxide in the airways. Thorax 2003;58:175-182.
[11] Nadeem A, Chhabra SK, Masood A, et al. Increased oxidative stress and altered levels of antioxidants in asthma. J Allergy Clin Immunol 2003;111:72-78.
[12] Monteseirin J, Bonilla I, Camacho J, et al. Elevated secretion of myeloperoxidase by neutrophils from asthmatic patients: the effect of immunotherapy. J Allergy Clin Immunol 2001;107:623-626.
[13] Kharitonov SA, Barnes PJ. Exhaled markers of pulmonary disease. Am J Respir Crit Care Med 2001;163:1693-1772.
[14] Kharitonov SA, Barnes PJ. Biomarkers of some pulmonary diseases in exhaled breath.Biomarkers 2002,7:1-32.
[15] Dweik RA, Comhair SA, Gaston B, et al. NO chemical events in the human airway during the immediate and antigen-indeced asthmatic response. Proc Natl Acad Sci USA 2001;98:2622-2627.
[16] Kaminsky DA, Mitchell J, Carroll N, et al. Nitrotyrosine formation in the airways and lung parenchyma of patients with asthma. J Allergy Clin Immunol 1999;104:747-754.
[17] Saleh D, Ernst P, Lim S, et al. Increased formation of the potent oxidant peroxynitrite in the airways of asthmatic patients is associated with induction 1998; 12:929-937.
[18] MacPherson JC, Comhair SA, Erzurum SC, et al. Eosinophils are a major source of nitric oxide-derived oxidants in severe asthma: characterization of pathways available to eosinophils for generating reactive nitrogen species. J Immunol 2001; 166:5763-5772.
[19] Wu W, Samoszuk MK, Comhair SA, et al. Eosinophils generate brominating oxidants inoxidants in allergen-induced asthma. J Clin Invest 2000;105:1455-1463.
[20] Gaston B, Seara S, Woods J, et al. Bronchodilator S-nitrosothiol deficiency in asthmatic respiratory failure. Lancet 1998;351:1317-1319.
[21] Puddicombe SM, Torres-Lozano C, Richter A, et al. Increased expreeion of p21(waf) cyclin-dependent kinase inhibitor in asthmatic bronchial epithelium. Am J Respir. Cell Mol Biol 2003;28:61-68.
[22] Comhair SA, Bhathena PR, Farver C, et al. Extracellular glutathione peroxidase induction in asthmatic lungs: evidence for redox regulation of expression in human airways epithelial cells. FASEB J 2001;15:70-78.
[23] Kaur B, Rowe BH, Ram FS. Vitamin C supplementation for asthma(Ccchrane Review). CochraneDatabase Syst Rev 2001;4:CD000993.
[24] Romieu I,Sienra-Monge JJ,Ramirez M, et al. Genetic polymorphism of GSTM1 and antioxidant supplementation influence lung function in relation to ozone exposure in asthmatic children in Mexico City. Thorax 2004;59:8-10.
[25] Romieu I, Sienra-Monge JJ, Ramire-Aguilar M, et al. Antioxidant supplementation and lung functions among children with asthma exposed to high levels of air pollutants. Am J Respir Crit Care Med 2002; 166:703-709.
[26] Wills-Karp M, Karp CL. Eosinophils in asthma: Romodeling a tangled tale. Science 2004;305(17):1726-1728.
[27] Wedi B, Straede J, Wieland B, et al. Blood 1999;94:2365-.
[28] Kankaanranta H, Giembycz MA, Barnes PJ, et al. Int. Arch. Allergy Immunol 2002;127:73-.
[29] De Souza PM, Kankaanranta H, Michael A, et al. Blood 2002,99:3432-.
[30] Druilhe A, Letuve S, Pretolani M, et al. Apoptosis 2003;8:481-.
[31] Gardai SJ, Hoontrakoon R, Goddard CD, et al. J. Immunol 2003,170:556-.
[32] Kharitonov S, Barnes PJ. Am. J. Respir. Crit. Care Med. 2001,164:727-.
[33] Lehtimaki L, Kankaanranta H, Saarelainen S, et al. Am. J. Respir. Crit. Care Med.2001;163:1557-.
[34] Moilanen E, Whittle B, Moncada S. In Inflammation: Basic Principles and Clinical Correlates; Gallin JI, Snyderman R, Eds.; Lippincott Williams & Wilkins: Philadelphia1999;787-.
[35] Hebestreit H, Dibbert B, Balatti I, et al. J. Exp.Med. 1998;187:415-425.
[36] Kankaanranta H, Moilanen E, Zhang X. Pharmacological regulation of human eosinophil apoptosis. Current drug targets-Inflammation & Allergy 2005;4:433-445.
[37] Watson WH, Yang X, Choi YE, et al. Thioredoxin and its role in toxicology. Toxicological Sciences 2004;78:3-14.
[38]Balcewicz-Sablinska MK, Wollman EE, Gorti R, et al. Human eosinophil cytotoxicity-enhancing factor. II. Multiple forms synthesized by U937 cells and their relationship to thioredoxin/adult T cell leukemia-derived factor. The Journal of Immunology 1991;147(7):2170-2174.
[39] Saitoh M. and Nishitoh H. et.al. Mammalian thioredoxin is a direct inhibitor of apoptosis signal-regulating kinase (ASK1) .EMBO J. 17, 2596-2606 (1998) .
[40] Yingmei Liu and Wang Min , Thioredoxin promotes ASK1 ubiquitination and Degradation to inhibit ASK1-mediiated apoptosis in a redox activity-independent manner. Circulation Research. June 28, 2002 ; 90: 1259-1266.
[41] Saitoh M, Nishitoh H, et.al. Mammalian thioredoxin is a direct inhibitor of apoptosis signal-regulating kinase (ASK) 1. EMBO J. 1998; 17:2596-2606.
[42] Gotoh Y, Cooper JA. Reactive oxygen species- and dimerization-induced activation of apoptosis signal-regulating kinase 1 in tumor necrosis factor-alpha signal transduction. J Biol Chem. 1998;273:17477-17482.
[43] Liu H, Nishitoh H et.al. Activation of apoptosis signalregulating kinase 1 (ASK1) by tumor necrosis factor receptor-associated factor 2 requires prior dissociation of the ASK1 inhibitor thioredoxin. Mol Cell Biol. 2000;20:2198-2208.
[44] Davis, R.J., MAPKs: new JNK expands the group.Trends Biochem.Sci.19, 470-473 (1994).
[45] Sapiro, L. and Dinarello, C.A., Osmotic Regulation of Cytokine Synthesis in vitro.Proc.Natl.Acad.Sci.USA.92, 12230-12234 (1995) .
[46] Hashimoto, S., Gon, Y., Matsumoto, K., Nakayama, T., Takeshita, L. and HorieT. Hyperosmolarity-induced Interleukin-8 Expression in Human Bronchial EpithelialCellsthroughp38Mitogen-activatedProteinKinase.AmJ.Respir.Crit.Care Med.159,634-640 (1999) .
[47] Shu Hashimoto, Ken Matsumoto, Yasuhiro Gon, Sachiko Furuichi, Shuichiro Maruoka Ikuko Takeshita, Kiichi Hirota, Junji Yodoi and Takashi Horie, Thioredoxin negatively regulates p38 MAP kinase activation and EL-6 production by tumor necrosis factor-α, Biochemical and Biophysical Research Communications 258, 443-447 (1999) .
[48] Kei Tobiume, et.al. ASK1 is required for sustained activations of JNK/p38 MAP kinases and apoptosis. EMBO reports vol.2 no.3 222-228 (2001) .
[49] Meier, B., Radeke, H.H., Selle, S., Younes, M., Sies, H., Resch, K. and Habermehl, G, Human fibroblasts release reactive oxygen species in response to interleukin-1 or tumour necrosis factor-alpha.Biochem.J.263, 539-545 (1989) .
[50] Schreck, R. and Baeuerle, P.A., A role for oxygen radicals as second messengers.Trend.Cell Biol.1, 39-42 (1991) .
[51] Saitoh, M., Nishitoh, H., Fujii, M., Takeda, K., Tobiume, K., Sawada, Y, Kawabata, M., Miyazono, K. and Ichijo, H., Mammalian thioredoxin is a direct inhibitor of apoptosis signal-regulating kinase (ASK) 1.EMBO J.17, 2596-2606 (1998) .
[52]Droge, W., Eck, H-P. and Mihm, S., HTV-induced cysteine deficiency and T-cell dysfunction—arationalefortreatment with N-acetylcysteine.Immunol.Todayl3,211-2(1992).
[53] Kiichi Hirota, Minoru Matsui, AP-1 transcriptional activity is regulated by a direct association between thioredoxin and Ref-1. Proc. Natl. Acad. Sci. USA Vol.94,pp.3633-3638, April 1997.
[54] Xanthoudakis, S., Miao, G.et.al. Redox activation of Fos-Jun DNA binding activity is mediated by a DNA repair enzyme.(1992) EMBO J. 11, 3323-3335.
[55] Pahl, H. L., and Baeuerle, P. A. Oxygen and the control of gene expression. (1994)BioEssays 16,497-502.
[56] Woronicz, J. D., et.al. IκB Kinase-P: NF-kB Activation and Complex Formation with IκB Kinase-α. and NIK .(1997) Science 278, 866-869.
[57] Nishiyama, A., et.al. Demonstration of the interaction of thioredoxin with p40phox, a phagocyte oxidase component, using a yeast two-hybrid system. (1999) Immunol. Lett. 68,155-159.
[58] Kiichi Hirota, Miyahiko Murata et.al. Distinct Roles of Thioredoxin in the Cytoplasm and in the Nucleus: A TWO-STEP MECHANISM OF REDOX REGULATION OF TRANSCRIPTION FACTOR NF-kB. THE JOURNAL OF BIOLOGICAL CHEMISTRY Vol. 274, No. 39, Issue of September 24, pp. 27891-27897, 1999.
[59] F Oehme, W Jonghaus, et.al.A nonradioactive 96-well plate assay for the detection of hypoxia-inducible factor prolyl hydroxylase activity.Anal Biochem, July 1, 2004;330(1):74-80.
[60] Kallio, P. J., Wilson, W. J., et.al.Regulation of the hypoxia-inducible factor-1_by the ubiquitin-proteasome pathway. J. Biol. Chem.,274: 6519-6525, 1999.
[61] Ema, M., Hirota, K., et.al. Molecular mechanisms of transcription activation by HLF and HIFl_in response to hypoxia: their stabilization and redox signal-induced interaction with CBP/p300. EMBO J., 18: 1905-1914, 1999.
[62] Sarah J. Welsh, et.al.The Redox Protein Thioredoxin-1 (Trx-1) Increases Hypoxia-inducible Factor 1_Protein Expression: Trx-1 Overexpression Results in Increased Vascular Endothelial Growth Factor Production and Enhanced Tumor Angiogenesis CANCER RESEARCH 62, 5089-5095, September 1, 2002.
[63] Grippo, J.F., et.al. 1985. Proof that the endogenous,heat-stable glucocorticoid receptor-activating factor is thioredoxin. J.Biol. Chem. 260:93-97.33. Sasada, T., S. Iwata,N.Sato,Y. Kitaoka,
[64] Yuichi Makino, et.al. Thioredoxin: a Redox-regulating Cellular Cofactor for Glucocorticoid Hormone Action:Cross Talk between Endocrine Control of Stress Response and Cellular Antioxidant Defense Systemv. J. Clin. Invest. Volume 98, Number 11, December 1996,2469-2477.
[65] Hirota, K., Matsui, M., Iwata, S., Nishiyama, A., Mori, K., and Yodoi, J. AP-1 transcriptional activity is regulated by a direct association between thioredoxin and Ref-1. Proc. Natl. Acad. Sci. U. S. A. 94, 3633-3638(1997).
[66] Masaya Ueno, Hiroshi Masutani(?),Thioredoxin-dependent Redox Regulation of p53-mediated p21 Activation Vol. 274, No. 50, Issue of December 10,pp. 35809-35815, 1999.
[67] Nishiyama A, Matsui M, Iwata S, Hirota K, Masutani H, Nakamura H, Takagi Y, Sono H,Gon Y, Yodoi J. Identification of thioredoxin-binding protein-2/vitamin D3 up-regulated protein 1 as a negative regulator of thioredoxin function and expression. J Biol Chem 1999;274:21645-21650.
[68] Anlin Wang, Gilles W. De Keulenaer, Richard T. Lee. Vitamin D3-up-regulated Protein Is a Stress-responsive Gene That Regulates Cardiomyocyte Viability through Interaction with Thioredoxin. J Biol Chem 2002;277:26496-26500.
[69] P.Christian Schulze, Gilles W. De Keulenaer, Jun Yoshioka, Kimbedy A. Kassik, Richard T. Lee. Vitamin D3-Upregulated Protein-1 (VDUP1) Regulates Redox-Dependent Vascular Smooth Muscle Cell Proliferation Through Interaction With Thioredoxin. Circulation Research 2002;91: 689-695.
[70] Yamawaki H, Pan S, Lee RT, et al. Fluid shear stress inhibits vascular inflammation by Decreasing thioredoxin-interacting protein in endothelial cells. The Journal of Clinical Investigation 2005; 115(3): 733-738.
[71] Yoshioka J, Schulze PC, Cupesi M, et al. Thioredoxin-interacting protein controls cardiac hypertrophy through regulation of thioredoxin activity. Circulation 2004; 109: 2581-2586.
[72] Minn AH, Hafele C, Shalev A. Thioredoxin-interacting protein is stimulated by glucose through a carbohydrate response element and induces β cell apoptosis. Endocrinology. First published February 10, 2005 as doi: 10.1210/en, 2004-1378.
[73] P. Christian Schulze, Jun Yoshioka, Tomosaburo Takahashi, Zhiheng He, George L. King, Richard T. Lee. Hyperglycemia Promotes Oxidative Stress through Inhibition of Thioredoxin Function by Thioredoxin-interacting Protein. J Biol Chem 2004;279: 30369—30374.
[74] Hui TY, Sheth SS, Diffley JM, et al. Mice lacking Thioredoxin-interacting protein provide Evidence linking cellular redox state to appropriate response to nutritional signals. Journal of Biol. Chem. 2004;279(23): 24387-24393.
[75] Jeon JH, Lee KN, Hwang CY, et al. Tumor suppressor VDUP1 increases p27~(kip1) stability by Inhibiting JAB 1. Cancer Res 2005;65(11): 4485-5589.
[76] Nishinaka Y, Nishiyama A, Masutani H, et al. Loss of Thioredoxin-binding protein-2/Vitamin D3-upregulated protein 1 in human T-cell leukemia virus type I-dependent T-cell transformation: implications for adult T-cell leukemia leukemogenesis. Cancet Research 2004;64(15): 1287-1292.
[77] C.E.Filby, S.B.Hooper, F.Sozo, V.A.Zahra, S.J.Flecknoe, M.J.Wallace. VDUP1: a potential mediator of expansion-induced lung growth and epithelial cell differentiation in the ovine fetus.AJP-Lung 2006;290: 250-258.
[78] 刘羽华，董亮程．诱导痰计数及其在评价气道炎症中的应用．中华结合和呼吸杂志2004；27(5)：336-339．
[79] 王彦，林强，王长征等．诱导痰的操作方法及其在哮喘中的应用．重庆医学2004；33(9)：1426-1428．
[80] TT Hansel, IJ De Vries, TIff, et al. An improved immunomagnetic procedure for the isolation of highly purified human blood eosinophils. J Immunol Methods 1991;15(12): 105-110.
[81] J Chihara, TB Nutman. Identification of eosinophils in lysed whole blood using side scatter and CD16 negativity. Cytometry 1997;30(6): 313-316.
[82] 赵海金，蔡绍曦，邹飞等．应用Super SMART cDNA Synthesis技术扩增哮喘嗜酸性粒细胞总RNA．第一军医大学学报2004；24(9)：1037-1039．
[83] FM Ducharme. Inhaled glucocorticoids versus leukotriene receptor antagonists as single agent asthma treatment: systematic review of current evidence. Biomedical Journal 2003;326(22):1-5.
[84] GE Vasso, KF Magne, T Masao, et al. Expression of activation markers and cytokine mRNA by peripheral blood CD4 and CD8 T cell atopic and nonatopic childhood asthma: effect of inhaled glucocirticoid therapy. Pediatrics 2002;109(2):1-9.
[85] PJ Bames. Corticosteroid effects on cell signalling. European Respiratory Journal 2006:27:413-426.
[86] Liu Y, Min W. Thioredoxin promotes ASK1 ubiquitination and degradation to inhibit ASK 1-mediated apoptosis in a redox activity-independent manner. Circulation Research 2002;90:1259-1266.
[87] Gotoh Y, Cooper JA. Reactive oxygen species and diamerization indeced activation of Apoptosis signal regulating kinase 1 in tumor necrosis factor a signal transduction. The Journal of Biological Chemnistry 1998;273(28):17477-17482.
[88] PS Steeg, T Ouatas, D Halverson, et al. Metastasis Suppressor Genes: Basic Biology and Potential Clinical Use Clin Breast Cancer 2003;4(1):51-62.
[89] Paul P., Tak, Gary S.Firestein. NF- κB : A Key Role in Inflammatory Diseases. The Journal of Clinical Investigation 2001;107:7-11.
[90] W Czech, J Krutmann, A Budnik, E Schopf, A Kapp. Induction of Intercellular Adhesion Molecule KICAM-I )Expression in Normal Human Eosinophils By Inflammatory Cytokines. J Invest Dermatol 1993;100(4):417-423.
[91] Mark A.Giembycz, Mark A.Lindsay. Pharmacology of the Eosinophil Pharmacological. Reviews 1999;51:213-340.
[1] Holmgren, A. Thioredoxin. Annu.Rev.Biochem.5 4, (1985) 237-271。
[2]A.Holmgren, Antioxidant function of thioredoxin and glutaredoxin systems, Antioxid, Redox Signal.2 (2000) 811-820.
[3]T.Tanaka, H.Nakamura, A.Nishiysma, F.Hosoi, H.Masutani, H.Wada and J.Yodoi, Redox regulation by thioredoxin superfamily: protection against oxidative stress and aging, Free Radic.Res.33 (2000), 851-855.
[4]Judith Haendeler, Jorg Hoffmann, Verena Tischler, Bradford C. Berkf, Andreas M. Zeiher and Stefanie Dimmeler, Redox regulatory and anti-apoptotic functions of thioredoxin depend on S-nitrosylation at cysteine 69, Nature Cell Biology, October 2002, vol4.
[5]Saitoh M. and Nishitoh H. et.al. Mammalian thioredoxin is a direct inhibitor of apoptosis signal-regulating kinase (ASKl) . EMBO J. 17, 2596-2606 (1998) .
[6]Yingmei Liu and Wang Min , Thioredoxin promotes ASKl ubiquitination and Degradation to inhibit ASKl-mediiated apoptosis in a redox activity-independent manner. Circulation Research. June 28, 2002 ; 90: 1259-1266.
[7]Saitoh M, Nishitoh H, et.al. Mammalian thioredoxin is a direct inhibitor of apoptosis signal-regulating kinase (ASK) 1. EMBO J. 1998; 17:2596-2606.
[8]Gotoh Y, Cooper JA. Reactive oxygen species- and dimerization-induced activation of apoptosis signal-regulating kinase 1 in tumor necrosis factor-alpha signal transduction. J Biol Chem. 1998;273:17477-17482.
[9] Liu H, Nishitoh H et.al. Activation of apoptosis signalregulating kinase 1 (ASKl) by tumor necrosis factor receptor-associated factor 2 requires prior dissociation of the ASKl inhibitor thioredoxin. Mol Cell Biol. 2000;20:2198-2208.
[10] Davis, R.J., MAPKs: new JNK expands the group.Trends Biochem.Sci.19, 470-473 (1994).
[11] Sapiro, L. and Dinarello, C.A. , Osmotic Regulation of Cytokine Synthesis in vitro.Proc.Natl.Acad.Sci.USA.92, 12230-12234 (1995) .
[12] Hashimoto, S., Gon, Y, Matsumoto, K., Nakayama, T., Takeshita, L. and Horie, T. , Hyperosmolarity-induced Interleukin-8 Expression in Human Bronchial EpithelialCellsthroughp38Mitogen-activatedProteinKinase.Am.J.Respir.Crit.Care Med.159, 634-640 (1999).
[13] Shu Hashimoto, Ken Matsumoto, Yasuhiro Gon, Sachiko Furuichi, Shuichiro Maruoka, Ikuko Takeshita, Kiichi Hirota, Junji Yodoi and Takashi Horie, Thioredoxin negatively regulates p38 MAP kinase activation and IL-6 production by tumor necrosis factor-α, Biochemical and Biophysical Research Communications 258, 443-447(1999).
[14] Kei Tobiume, et.al. ASK1 is required for sustained activations of JNK/p38 MAP kinases and apoptosis. EMBO reports vol.2 no.3 222-228 (2001).
[15] Meier, B., Radeke, H.H., Selle, S., Younes, M., Sies, H., Resch, K. and Habermehl, G., Human fibroblasts release reactive oxygen species in response to interleukin-1 or tumour necrosis factor-alpha. Biochem.J.263, 539-545(1989).
[16] Schreck, R. and Baeuerle, P.A., A role for oxygen radicals as second messengers.Trend.Cell Biol.1, 39-42(1991).
[17] Saitoh, M., Nishitoh, H., Fujii, M., Takeda, K., Tobiume, K., Sawada, Y., Kawabata, M., Miyazono, K. and Ichijo, H., Mammalian thioredoxin is a direct inhibitor of apoptosis signal-regulating kinase (ASK) 1. EMBO J.17, 2596-2606 (1998).
[18] Droge, W., Eck, H-P. and Mihm, S., HIV-induced cysteine deficiency and T-cell dysfunction—arationalefortreatment with N-acetylcysteine.Immunol.Today13, 211-214(1992).
[19] Kiichi Hirota, Minoru Matsui, AP-1 transcriptional activity is regulated by a direct association between thioredoxin and Ref-1. Proc. Natl. Acad. Sci. USA Vol. 94, pp. 3633-3638, April 1997.
[20] Xanthoudakis, S., Miao, G.et.al. Redox activation of Fos-Jun DNA binding activity is mediated by a DNA repair enzyme.(1992) EMBO J. 11, 3323-3335.
[21] Pahl, H. L., and Baeuerle, P. A. Oxygen and the control of gene expression. (1994) BioEssays 16, 497-502.
[22] Woronicz, J. D., et.al. IκB Kinase-β: NF-κB Activation and Complex Formation with IκB Kinase-α and NIK. (1997) Science 278, 866-869.
[23] Nishiyama, A., et.al. Demonstration of the interaction of thioredoxin with p40phox, a phagocyte oxidase component, using a yeast two-hybrid system. (1999) Immunol. Lett. 68,155-159.
[24] Kiichi Hirota, Miyahiko Murata et.al. Distinct Roles of Thioredoxin in the Cytoplasm and in the Nucleus: A TWO-STEP MECHANISM OF REDOX REGULATION OF TRANSCRIPTION FACTOR NF-kB.THE JOURNAL OF BIOLOGICAL
CHEMISTRY, Vol. 274, No. 39, Issue of September 24, pp. 27891-27897, 1999.
[25] F Oehme, W Jonghaus, et.al.A nonradioactive 96-well plate assay for the detection of hypoxia-inducible factor prolyl hydroxylase activity.Anal Biochem, July 1, 2004; 330(1): 74-80.
[26] Kallio, P. J., Wilson, W. J., et.al.Regulation of the hypoxia-inducible factor-l_by the ubiquitin-proteasome pathway. J. Biol. Chem.,274: 6519-6525, 1999.
[27] Ema, M., Hirota, K., et.al. Molecular mechanisms of transcription activation by HLF and HIFl_in response to hypoxia: their stabilization and redox signal-induced interaction with CBP/p300. EMBO J., 18: 1905-1914, 1999.
[28] Sarah J. Welsh, et.al.The Redox Protein Thioredoxin-1 (Trx-1) Increases Hypoxia-inducible Factor l_Protein Expression: Trx-1 Overexpression Results in Increased Vascular Endothelial Growth Factor Production and Enhanced Tumor Angiogenesis CANCER RESEARCH 62, 5089-5095, September 1, 2002.
[29] Grippo, J.F., et.al. 1985. Proof that the endogenous,heat-stable glucocorticoid receptor-activating factor is thioredoxin. J.Biol. Chem. 260:93-97.33. Sasada, T., S. Iwata,N. Sato, Y. Kitaoka,
[30] Yuichi Makino, et.al. Thioredoxin: a Redox-regulating Cellular Cofactor for Glucocorticoid Hormone Action:Cross Talk between Endocrine Control of Stress Response and Cellular Antioxidant Defense Systemv. J. Clin. Invest. Volume 98, Number 11, December 1996, 2469-2477.
[31] Hirota, K., Matsui, M., Iwata, S., Nishiyama, A., Mori, K., and Yodoi, J. AP-1 transcriptional activity is regulated by a direct association between thioredoxin and Ref-1. Proc. Natl. Acad. Sci. U. S. A. 94, 3633-3638(1997).
[32] Masaya Ueno≠§, Hiroshi Masutani≠, Thioredoxin-dependent Redox Regulation of p53-mediated p21. Activation Vol. 274, No. 50, Issue of December 10, pp. 35809-35815, 1999.
[2] Dworski R. Oxidant stress in asthma. Thorax 2000,55:51-53.
[3] Barnes PJ. Reactive oxygen species and airway inflammation. Free Redic Biol Med 1990;9:235-243.
[4] Barnes PJ, Chung KF, Page CP. Inflammatory mediators of asthma: on update. Pharmacol Rev 1998;50:515-596.
[5] Bowler RP, Crapo JD. Oxidative stress in allergic respiratory diseases. J Allergy Clin Immunol 2002;110:349-356.
[6] Dworski R. Oxidant stress in asthma. Thorax 2000;55(2):S51-S53.
[7] Henricks PA, Nijkamp FP. Reactive oxygen species as mediators in asthma. Pulm Pharmacol Ther 2001; 14:409-420.
[8] Rahman I, MacNee W. Reactive oxygen species. In: Barnes PJ, Drazen J, Rennard S,et al, eds. Asthma and COPD. London: Academic Press 2002:243-254.
[9] Aldridge RE, Chan T, van Dalen CJ, et al. Eosinophil peroxidase produces hypobromous acid in the airways of stable asthmatics. Free Radic Biol Med 2002;33:847-856.
[10] Ricciardolo FL. Multiple roles of nitric oxide in the airways. Thorax 2003;58:175-182.
[11] Nadeem A, Chhabra SK, Masood A, et al. Increased oxidative stress and altered levels of antioxidants in asthma. J Allergy Clin Immunol 2003;111:72-78.
[12] Monteseirin J, Bonilla I, Camacho J, et al. Elevated secretion of myeloperoxidase by neutrophils from asthmatic patients: the effect of immunotherapy. J Allergy Clin Immunol 2001;107:623-626.
[13] Kharitonov SA, Barnes PJ. Exhaled markers of pulmonary disease. Am J Respir Crit Care Med 2001;163:1693-1772.
[14] Kharitonov SA, Barnes PJ. Biomarkers of some pulmonary diseases in exhaled breath.Biomarkers 2002,7:1-32.
[15] Dweik RA, Comhair SA, Gaston B, et al. NO chemical events in the human airway during the immediate and antigen-indeced asthmatic response. Proc Natl Acad Sci USA 2001;98:2622-2627.
[16] Kaminsky DA, Mitchell J, Carroll N, et al. Nitrotyrosine formation in the airways and lung parenchyma of patients with asthma. J Allergy Clin Immunol 1999;104:747-754.
[17] Saleh D, Ernst P, Lim S, et al. Increased formation of the potent oxidant peroxynitrite in the airways of asthmatic patients is associated with induction 1998; 12:929-937.
[18] MacPherson JC, Comhair SA, Erzurum SC, et al. Eosinophils are a major source of nitric oxide-derived oxidants in severe asthma: characterization of pathways available to eosinophils for generating reactive nitrogen species. J Immunol 2001; 166:5763-5772.
[19] Wu W, Samoszuk MK, Comhair SA, et al. Eosinophils generate brominating oxidants inoxidants in allergen-induced asthma. J Clin Invest 2000;105:1455-1463.
[20] Gaston B, Seara S, Woods J, et al. Bronchodilator S-nitrosothiol deficiency in asthmatic respiratory failure. Lancet 1998;351:1317-1319.
[21] Puddicombe SM, Torres-Lozano C, Richter A, et al. Increased expreeion of p21(waf) cyclin-dependent kinase inhibitor in asthmatic bronchial epithelium. Am J Respir. Cell Mol Biol 2003;28:61-68.
[22] Comhair SA, Bhathena PR, Farver C, et al. Extracellular glutathione peroxidase induction in asthmatic lungs: evidence for redox regulation of expression in human airways epithelial cells. FASEB J 2001;15:70-78.
[23] Kaur B, Rowe BH, Ram FS. Vitamin C supplementation for asthma(Ccchrane Review). CochraneDatabase Syst Rev 2001;4:CD000993.
[24] Romieu I,Sienra-Monge JJ,Ramirez M, et al. Genetic polymorphism of GSTM1 and antioxidant supplementation influence lung function in relation to ozone exposure in asthmatic children in Mexico City. Thorax 2004;59:8-10.
[25] Romieu I, Sienra-Monge JJ, Ramire-Aguilar M, et al. Antioxidant supplementation and lung functions among children with asthma exposed to high levels of air pollutants. Am J Respir Crit Care Med 2002; 166:703-709.
[26] Wills-Karp M, Karp CL. Eosinophils in asthma: Romodeling a tangled tale. Science 2004;305(17):1726-1728.
[27] Wedi B, Straede J, Wieland B, et al. Blood 1999;94:2365-.
[28] Kankaanranta H, Giembycz MA, Barnes PJ, et al. Int. Arch. Allergy Immunol 2002;127:73-.
[29] De Souza PM, Kankaanranta H, Michael A, et al. Blood 2002,99:3432-.
[30] Druilhe A, Letuve S, Pretolani M, et al. Apoptosis 2003;8:481-.
[31] Gardai SJ, Hoontrakoon R, Goddard CD, et al. J. Immunol 2003,170:556-.
[32] Kharitonov S, Barnes PJ. Am. J. Respir. Crit. Care Med. 2001,164:727-.
[33] Lehtimaki L, Kankaanranta H, Saarelainen S, et al. Am. J. Respir. Crit. Care Med.2001;163:1557-.
[34] Moilanen E, Whittle B, Moncada S. In Inflammation: Basic Principles and Clinical Correlates; Gallin JI, Snyderman R, Eds.; Lippincott Williams & Wilkins: Philadelphia1999;787-.
[35] Hebestreit H, Dibbert B, Balatti I, et al. J. Exp.Med. 1998;187:415-425.
[36] Kankaanranta H, Moilanen E, Zhang X. Pharmacological regulation of human eosinophil apoptosis. Current drug targets-Inflammation & Allergy 2005;4:433-445.
[37] Watson WH, Yang X, Choi YE, et al. Thioredoxin and its role in toxicology. Toxicological Sciences 2004;78:3-14.
[38]Balcewicz-Sablinska MK, Wollman EE, Gorti R, et al. Human eosinophil cytotoxicity-enhancing factor. II. Multiple forms synthesized by U937 cells and their relationship to thioredoxin/adult T cell leukemia-derived factor. The Journal of Immunology 1991;147(7):2170-2174.
[39] Saitoh M. and Nishitoh H. et.al. Mammalian thioredoxin is a direct inhibitor of apoptosis signal-regulating kinase (ASK1) .EMBO J. 17, 2596-2606 (1998) .
[40] Yingmei Liu and Wang Min , Thioredoxin promotes ASK1 ubiquitination and Degradation to inhibit ASK1-mediiated apoptosis in a redox activity-independent manner. Circulation Research. June 28, 2002 ; 90: 1259-1266.
[41] Saitoh M, Nishitoh H, et.al. Mammalian thioredoxin is a direct inhibitor of apoptosis signal-regulating kinase (ASK) 1. EMBO J. 1998; 17:2596-2606.
[42] Gotoh Y, Cooper JA. Reactive oxygen species- and dimerization-induced activation of apoptosis signal-regulating kinase 1 in tumor necrosis factor-alpha signal transduction. J Biol Chem. 1998;273:17477-17482.
[43] Liu H, Nishitoh H et.al. Activation of apoptosis signalregulating kinase 1 (ASK1) by tumor necrosis factor receptor-associated factor 2 requires prior dissociation of the ASK1 inhibitor thioredoxin. Mol Cell Biol. 2000;20:2198-2208.
[44] Davis, R.J., MAPKs: new JNK expands the group.Trends Biochem.Sci.19, 470-473 (1994).
[45] Sapiro, L. and Dinarello, C.A., Osmotic Regulation of Cytokine Synthesis in vitro.Proc.Natl.Acad.Sci.USA.92, 12230-12234 (1995) .
[46] Hashimoto, S., Gon, Y., Matsumoto, K., Nakayama, T., Takeshita, L. and HorieT. Hyperosmolarity-induced Interleukin-8 Expression in Human Bronchial EpithelialCellsthroughp38Mitogen-activatedProteinKinase.AmJ.Respir.Crit.Care Med.159,634-640 (1999) .
[47] Shu Hashimoto, Ken Matsumoto, Yasuhiro Gon, Sachiko Furuichi, Shuichiro Maruoka Ikuko Takeshita, Kiichi Hirota, Junji Yodoi and Takashi Horie, Thioredoxin negatively regulates p38 MAP kinase activation and EL-6 production by tumor necrosis factor-α, Biochemical and Biophysical Research Communications 258, 443-447 (1999) .
[48] Kei Tobiume, et.al. ASK1 is required for sustained activations of JNK/p38 MAP kinases and apoptosis. EMBO reports vol.2 no.3 222-228 (2001) .
[49] Meier, B., Radeke, H.H., Selle, S., Younes, M., Sies, H., Resch, K. and Habermehl, G, Human fibroblasts release reactive oxygen species in response to interleukin-1 or tumour necrosis factor-alpha.Biochem.J.263, 539-545 (1989) .
[50] Schreck, R. and Baeuerle, P.A., A role for oxygen radicals as second messengers.Trend.Cell Biol.1, 39-42 (1991) .
[51] Saitoh, M., Nishitoh, H., Fujii, M., Takeda, K., Tobiume, K., Sawada, Y, Kawabata, M., Miyazono, K. and Ichijo, H., Mammalian thioredoxin is a direct inhibitor of apoptosis signal-regulating kinase (ASK) 1.EMBO J.17, 2596-2606 (1998) .
[52]Droge, W., Eck, H-P. and Mihm, S., HTV-induced cysteine deficiency and T-cell dysfunction—arationalefortreatment with N-acetylcysteine.Immunol.Todayl3,211-2(1992).
[53] Kiichi Hirota, Minoru Matsui, AP-1 transcriptional activity is regulated by a direct association between thioredoxin and Ref-1. Proc. Natl. Acad. Sci. USA Vol.94,pp.3633-3638, April 1997.
[54] Xanthoudakis, S., Miao, G.et.al. Redox activation of Fos-Jun DNA binding activity is mediated by a DNA repair enzyme.(1992) EMBO J. 11, 3323-3335.
[55] Pahl, H. L., and Baeuerle, P. A. Oxygen and the control of gene expression. (1994)BioEssays 16,497-502.
[56] Woronicz, J. D., et.al. IκB Kinase-P: NF-kB Activation and Complex Formation with IκB Kinase-α. and NIK .(1997) Science 278, 866-869.
[57] Nishiyama, A., et.al. Demonstration of the interaction of thioredoxin with p40phox, a phagocyte oxidase component, using a yeast two-hybrid system. (1999) Immunol. Lett. 68,155-159.
[58] Kiichi Hirota, Miyahiko Murata et.al. Distinct Roles of Thioredoxin in the Cytoplasm and in the Nucleus: A TWO-STEP MECHANISM OF REDOX REGULATION OF TRANSCRIPTION FACTOR NF-kB. THE JOURNAL OF BIOLOGICAL CHEMISTRY Vol. 274, No. 39, Issue of September 24, pp. 27891-27897, 1999.
[59] F Oehme, W Jonghaus, et.al.A nonradioactive 96-well plate assay for the detection of hypoxia-inducible factor prolyl hydroxylase activity.Anal Biochem, July 1, 2004;330(1):74-80.
[60] Kallio, P. J., Wilson, W. J., et.al.Regulation of the hypoxia-inducible factor-1_by the ubiquitin-proteasome pathway. J. Biol. Chem.,274: 6519-6525, 1999.
[61] Ema, M., Hirota, K., et.al. Molecular mechanisms of transcription activation by HLF and HIFl_in response to hypoxia: their stabilization and redox signal-induced interaction with CBP/p300. EMBO J., 18: 1905-1914, 1999.
[62] Sarah J. Welsh, et.al.The Redox Protein Thioredoxin-1 (Trx-1) Increases Hypoxia-inducible Factor 1_Protein Expression: Trx-1 Overexpression Results in Increased Vascular Endothelial Growth Factor Production and Enhanced Tumor Angiogenesis CANCER RESEARCH 62, 5089-5095, September 1, 2002.
[63] Grippo, J.F., et.al. 1985. Proof that the endogenous,heat-stable glucocorticoid receptor-activating factor is thioredoxin. J.Biol. Chem. 260:93-97.33. Sasada, T., S. Iwata,N.Sato,Y. Kitaoka,
[64] Yuichi Makino, et.al. Thioredoxin: a Redox-regulating Cellular Cofactor for Glucocorticoid Hormone Action:Cross Talk between Endocrine Control of Stress Response and Cellular Antioxidant Defense Systemv. J. Clin. Invest. Volume 98, Number 11, December 1996,2469-2477.
[65] Hirota, K., Matsui, M., Iwata, S., Nishiyama, A., Mori, K., and Yodoi, J. AP-1 transcriptional activity is regulated by a direct association between thioredoxin and Ref-1. Proc. Natl. Acad. Sci. U. S. A. 94, 3633-3638(1997).
[66] Masaya Ueno, Hiroshi Masutani(?),Thioredoxin-dependent Redox Regulation of p53-mediated p21 Activation Vol. 274, No. 50, Issue of December 10,pp. 35809-35815, 1999.
[67] Nishiyama A, Matsui M, Iwata S, Hirota K, Masutani H, Nakamura H, Takagi Y, Sono H,Gon Y, Yodoi J. Identification of thioredoxin-binding protein-2/vitamin D3 up-regulated protein 1 as a negative regulator of thioredoxin function and expression. J Biol Chem 1999;274:21645-21650.
[68] Anlin Wang, Gilles W. De Keulenaer, Richard T. Lee. Vitamin D3-up-regulated Protein Is a Stress-responsive Gene That Regulates Cardiomyocyte Viability through Interaction with Thioredoxin. J Biol Chem 2002;277:26496-26500.
[69] P.Christian Schulze, Gilles W. De Keulenaer, Jun Yoshioka, Kimbedy A. Kassik, Richard T. Lee. Vitamin D3-Upregulated Protein-1 (VDUP1) Regulates Redox-Dependent Vascular Smooth Muscle Cell Proliferation Through Interaction With Thioredoxin. Circulation Research 2002;91: 689-695.
[70] Yamawaki H, Pan S, Lee RT, et al. Fluid shear stress inhibits vascular inflammation by Decreasing thioredoxin-interacting protein in endothelial cells. The Journal of Clinical Investigation 2005; 115(3): 733-738.
[71] Yoshioka J, Schulze PC, Cupesi M, et al. Thioredoxin-interacting protein controls cardiac hypertrophy through regulation of thioredoxin activity. Circulation 2004; 109: 2581-2586.
[72] Minn AH, Hafele C, Shalev A. Thioredoxin-interacting protein is stimulated by glucose through a carbohydrate response element and induces β cell apoptosis. Endocrinology. First published February 10, 2005 as doi: 10.1210/en, 2004-1378.
[73] P. Christian Schulze, Jun Yoshioka, Tomosaburo Takahashi, Zhiheng He, George L. King, Richard T. Lee. Hyperglycemia Promotes Oxidative Stress through Inhibition of Thioredoxin Function by Thioredoxin-interacting Protein. J Biol Chem 2004;279: 30369—30374.
[74] Hui TY, Sheth SS, Diffley JM, et al. Mice lacking Thioredoxin-interacting protein provide Evidence linking cellular redox state to appropriate response to nutritional signals. Journal of Biol. Chem. 2004;279(23): 24387-24393.
[75] Jeon JH, Lee KN, Hwang CY, et al. Tumor suppressor VDUP1 increases p27~(kip1) stability by Inhibiting JAB 1. Cancer Res 2005;65(11): 4485-5589.
[76] Nishinaka Y, Nishiyama A, Masutani H, et al. Loss of Thioredoxin-binding protein-2/Vitamin D3-upregulated protein 1 in human T-cell leukemia virus type I-dependent T-cell transformation: implications for adult T-cell leukemia leukemogenesis. Cancet Research 2004;64(15): 1287-1292.
[77] C.E.Filby, S.B.Hooper, F.Sozo, V.A.Zahra, S.J.Flecknoe, M.J.Wallace. VDUP1: a potential mediator of expansion-induced lung growth and epithelial cell differentiation in the ovine fetus.AJP-Lung 2006;290: 250-258.
[78] 刘羽华，董亮程．诱导痰计数及其在评价气道炎症中的应用．中华结合和呼吸杂志2004；27(5)：336-339．
[79] 王彦，林强，王长征等．诱导痰的操作方法及其在哮喘中的应用．重庆医学2004；33(9)：1426-1428．
[80] TT Hansel, IJ De Vries, TIff, et al. An improved immunomagnetic procedure for the isolation of highly purified human blood eosinophils. J Immunol Methods 1991;15(12): 105-110.
[81] J Chihara, TB Nutman. Identification of eosinophils in lysed whole blood using side scatter and CD16 negativity. Cytometry 1997;30(6): 313-316.
[82] 赵海金，蔡绍曦，邹飞等．应用Super SMART cDNA Synthesis技术扩增哮喘嗜酸性粒细胞总RNA．第一军医大学学报2004；24(9)：1037-1039．
[83] FM Ducharme. Inhaled glucocorticoids versus leukotriene receptor antagonists as single agent asthma treatment: systematic review of current evidence. Biomedical Journal 2003;326(22):1-5.
[84] GE Vasso, KF Magne, T Masao, et al. Expression of activation markers and cytokine mRNA by peripheral blood CD4 and CD8 T cell atopic and nonatopic childhood asthma: effect of inhaled glucocirticoid therapy. Pediatrics 2002;109(2):1-9.
[85] PJ Bames. Corticosteroid effects on cell signalling. European Respiratory Journal 2006:27:413-426.
[86] Liu Y, Min W. Thioredoxin promotes ASK1 ubiquitination and degradation to inhibit ASK 1-mediated apoptosis in a redox activity-independent manner. Circulation Research 2002;90:1259-1266.
[87] Gotoh Y, Cooper JA. Reactive oxygen species and diamerization indeced activation of Apoptosis signal regulating kinase 1 in tumor necrosis factor a signal transduction. The Journal of Biological Chemnistry 1998;273(28):17477-17482.
[88] PS Steeg, T Ouatas, D Halverson, et al. Metastasis Suppressor Genes: Basic Biology and Potential Clinical Use Clin Breast Cancer 2003;4(1):51-62.
[89] Paul P., Tak, Gary S.Firestein. NF- κB : A Key Role in Inflammatory Diseases. The Journal of Clinical Investigation 2001;107:7-11.
[90] W Czech, J Krutmann, A Budnik, E Schopf, A Kapp. Induction of Intercellular Adhesion Molecule KICAM-I )Expression in Normal Human Eosinophils By Inflammatory Cytokines. J Invest Dermatol 1993;100(4):417-423.
[91] Mark A.Giembycz, Mark A.Lindsay. Pharmacology of the Eosinophil Pharmacological. Reviews 1999;51:213-340.
[1] Holmgren, A. Thioredoxin. Annu.Rev.Biochem.5 4, (1985) 237-271。
[2]A.Holmgren, Antioxidant function of thioredoxin and glutaredoxin systems, Antioxid, Redox Signal.2 (2000) 811-820.
[3]T.Tanaka, H.Nakamura, A.Nishiysma, F.Hosoi, H.Masutani, H.Wada and J.Yodoi, Redox regulation by thioredoxin superfamily: protection against oxidative stress and aging, Free Radic.Res.33 (2000), 851-855.
[4]Judith Haendeler, Jorg Hoffmann, Verena Tischler, Bradford C. Berkf, Andreas M. Zeiher and Stefanie Dimmeler, Redox regulatory and anti-apoptotic functions of thioredoxin depend on S-nitrosylation at cysteine 69, Nature Cell Biology, October 2002, vol4.
[5]Saitoh M. and Nishitoh H. et.al. Mammalian thioredoxin is a direct inhibitor of apoptosis signal-regulating kinase (ASKl) . EMBO J. 17, 2596-2606 (1998) .
[6]Yingmei Liu and Wang Min , Thioredoxin promotes ASKl ubiquitination and Degradation to inhibit ASKl-mediiated apoptosis in a redox activity-independent manner. Circulation Research. June 28, 2002 ; 90: 1259-1266.
[7]Saitoh M, Nishitoh H, et.al. Mammalian thioredoxin is a direct inhibitor of apoptosis signal-regulating kinase (ASK) 1. EMBO J. 1998; 17:2596-2606.
[8]Gotoh Y, Cooper JA. Reactive oxygen species- and dimerization-induced activation of apoptosis signal-regulating kinase 1 in tumor necrosis factor-alpha signal transduction. J Biol Chem. 1998;273:17477-17482.
[9] Liu H, Nishitoh H et.al. Activation of apoptosis signalregulating kinase 1 (ASKl) by tumor necrosis factor receptor-associated factor 2 requires prior dissociation of the ASKl inhibitor thioredoxin. Mol Cell Biol. 2000;20:2198-2208.
[10] Davis, R.J., MAPKs: new JNK expands the group.Trends Biochem.Sci.19, 470-473 (1994).
[11] Sapiro, L. and Dinarello, C.A. , Osmotic Regulation of Cytokine Synthesis in vitro.Proc.Natl.Acad.Sci.USA.92, 12230-12234 (1995) .
[12] Hashimoto, S., Gon, Y, Matsumoto, K., Nakayama, T., Takeshita, L. and Horie, T. , Hyperosmolarity-induced Interleukin-8 Expression in Human Bronchial EpithelialCellsthroughp38Mitogen-activatedProteinKinase.Am.J.Respir.Crit.Care Med.159, 634-640 (1999).
[13] Shu Hashimoto, Ken Matsumoto, Yasuhiro Gon, Sachiko Furuichi, Shuichiro Maruoka, Ikuko Takeshita, Kiichi Hirota, Junji Yodoi and Takashi Horie, Thioredoxin negatively regulates p38 MAP kinase activation and IL-6 production by tumor necrosis factor-α, Biochemical and Biophysical Research Communications 258, 443-447(1999).
[14] Kei Tobiume, et.al. ASK1 is required for sustained activations of JNK/p38 MAP kinases and apoptosis. EMBO reports vol.2 no.3 222-228 (2001).
[15] Meier, B., Radeke, H.H., Selle, S., Younes, M., Sies, H., Resch, K. and Habermehl, G., Human fibroblasts release reactive oxygen species in response to interleukin-1 or tumour necrosis factor-alpha. Biochem.J.263, 539-545(1989).
[16] Schreck, R. and Baeuerle, P.A., A role for oxygen radicals as second messengers.Trend.Cell Biol.1, 39-42(1991).
[17] Saitoh, M., Nishitoh, H., Fujii, M., Takeda, K., Tobiume, K., Sawada, Y., Kawabata, M., Miyazono, K. and Ichijo, H., Mammalian thioredoxin is a direct inhibitor of apoptosis signal-regulating kinase (ASK) 1. EMBO J.17, 2596-2606 (1998).
[18] Droge, W., Eck, H-P. and Mihm, S., HIV-induced cysteine deficiency and T-cell dysfunction—arationalefortreatment with N-acetylcysteine.Immunol.Today13, 211-214(1992).
[19] Kiichi Hirota, Minoru Matsui, AP-1 transcriptional activity is regulated by a direct association between thioredoxin and Ref-1. Proc. Natl. Acad. Sci. USA Vol. 94, pp. 3633-3638, April 1997.
[20] Xanthoudakis, S., Miao, G.et.al. Redox activation of Fos-Jun DNA binding activity is mediated by a DNA repair enzyme.(1992) EMBO J. 11, 3323-3335.
[21] Pahl, H. L., and Baeuerle, P. A. Oxygen and the control of gene expression. (1994) BioEssays 16, 497-502.
[22] Woronicz, J. D., et.al. IκB Kinase-β: NF-κB Activation and Complex Formation with IκB Kinase-α and NIK. (1997) Science 278, 866-869.
[23] Nishiyama, A., et.al. Demonstration of the interaction of thioredoxin with p40phox, a phagocyte oxidase component, using a yeast two-hybrid system. (1999) Immunol. Lett. 68,155-159.
[24] Kiichi Hirota, Miyahiko Murata et.al. Distinct Roles of Thioredoxin in the Cytoplasm and in the Nucleus: A TWO-STEP MECHANISM OF REDOX REGULATION OF TRANSCRIPTION FACTOR NF-kB.THE JOURNAL OF BIOLOGICAL
CHEMISTRY, Vol. 274, No. 39, Issue of September 24, pp. 27891-27897, 1999.
[25] F Oehme, W Jonghaus, et.al.A nonradioactive 96-well plate assay for the detection of hypoxia-inducible factor prolyl hydroxylase activity.Anal Biochem, July 1, 2004; 330(1): 74-80.
[26] Kallio, P. J., Wilson, W. J., et.al.Regulation of the hypoxia-inducible factor-l_by the ubiquitin-proteasome pathway. J. Biol. Chem.,274: 6519-6525, 1999.
[27] Ema, M., Hirota, K., et.al. Molecular mechanisms of transcription activation by HLF and HIFl_in response to hypoxia: their stabilization and redox signal-induced interaction with CBP/p300. EMBO J., 18: 1905-1914, 1999.
[28] Sarah J. Welsh, et.al.The Redox Protein Thioredoxin-1 (Trx-1) Increases Hypoxia-inducible Factor l_Protein Expression: Trx-1 Overexpression Results in Increased Vascular Endothelial Growth Factor Production and Enhanced Tumor Angiogenesis CANCER RESEARCH 62, 5089-5095, September 1, 2002.
[29] Grippo, J.F., et.al. 1985. Proof that the endogenous,heat-stable glucocorticoid receptor-activating factor is thioredoxin. J.Biol. Chem. 260:93-97.33. Sasada, T., S. Iwata,N. Sato, Y. Kitaoka,
[30] Yuichi Makino, et.al. Thioredoxin: a Redox-regulating Cellular Cofactor for Glucocorticoid Hormone Action:Cross Talk between Endocrine Control of Stress Response and Cellular Antioxidant Defense Systemv. J. Clin. Invest. Volume 98, Number 11, December 1996, 2469-2477.
[31] Hirota, K., Matsui, M., Iwata, S., Nishiyama, A., Mori, K., and Yodoi, J. AP-1 transcriptional activity is regulated by a direct association between thioredoxin and Ref-1. Proc. Natl. Acad. Sci. U. S. A. 94, 3633-3638(1997).
[32] Masaya Ueno≠§, Hiroshi Masutani≠, Thioredoxin-dependent Redox Regulation of p53-mediated p21. Activation Vol. 274, No. 50, Issue of December 10, pp. 35809-35815, 1999.