Apoptosis inhibitor of macrophage (AIM) expression in alveolar macrophages in COPD

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• 作者：Jun Kojima (1)
  Jun Araya (1)
  Hiromichi Hara (1)
  Saburo Ito (1)
  Naoki Takasaka (1)
  Kenji Kobayashi (1)
  Satoko Fujii (1)
  Chikako Tsurushige (1)
  Takanori Numata (1)
  Takeo Ishikawa (1)
  Kenichiro Shimizu (1)
  Makoto Kawaishi (1)
  Keisuke Saito (1)
  Noriki Kamiya (2)
  Jun Hirano (2)
  Makoto Odaka (2)
  Toshiaki Morikawa (2)
  Hiroshi Hano (3)
  Satoko Arai (4)
  Toru Miyazaki (4)
  Yumi Kaneko (1)
  Katsutoshi Nakayama (1)
  Kazuyoshi Kuwano (1)
  
• 关键词：AIM ; Alveolar macrophage ; Apoptosis ; COPD
• 刊名：Respiratory Research
• 出版年：2013
• 出版时间：December 2013
• 年：2013
• 卷：14
• 期：1
• 全文大小：596KB
• 参考文献：1. Eisner MD, Anthonisen N, Coultas D, Kuenzli N, Perez-Padilla R, Postma D, Romieu I, Silverman EK, Balmes JR: An official american thoracic society public policy statement: novel risk factors and the global burden of chronic obstructive pulmonary disease. / Am J Respir Crit Care Med 2010,182(5):693-18. CrossRef
  2. Barnes PJ: Alveolar macrophages as orchestrators of COPD. / COPD 2004, 1:59-0. CrossRef
  3. Tetley TD: Macrophages and the pathogenesis of COPD. / Chest 2002,121(5 Suppl):156S-159S. CrossRef
  4. Brusselle GG, Joos GF, Bracke KR: New insights into the immunology of chronic obstructive pulmonary disease. / Lancet 2011,378(9795):1015-026. CrossRef
  5. Barnes PJ: Immunology of asthma and chronic obstructive pulmonary disease. / Nat Rev Immunol 2008,8(3):183-92. CrossRef
  6. Di Stefano A, Capelli A, Lusuardi M, Balbo P, Vecchio C, Maestrelli P, Mapp CE, Fabbri LM, Donner CF, Saetta M: Severity of airflow limitation is associated with severity of airway inflammation in smokers. / Am J Respir Crit Care Med 1998, 158:1277-285.
  7. Vlahos R, Bozinovski S, Chan SP, Ivanov S, Lindén A, Hamilton JA, Anderson GP: Neutralizing granulocyte/macrophage colony-stimulating factor inhibits cigarette smoke-induced lung inflammation. / Am J Respir Crit Care Med 2010, 182:34-0. CrossRef
  8. Kuwano K, Araya J, Nakayama K: Epithelial cell fate following lung injury. / Expert Rev Respir Med 2008,2(5):573-82. CrossRef
  9. Kasahara Y, Tuder RM, Taraseviciene-Stewart L, Le Cras TD, Abman S, Hirth PK, Waltenberger J, Voelkel NF: Inhibition of VEGF receptors causes lung cell apoptosis and emphysema. / J Clin Invest 2000,106(11):1311-319. CrossRef
  10. Siganaki M, Koutsopoulos AV, Neofytou E, Vlachaki E, Psarrou M, Soulitzis N, Pentilas N, Schiza S, Siafakas NM, Tzortzaki EG: Deregulation of apoptosis mediators-p53 and bcl2 in lung tissue of copd patients. / Respir Res 2010, 11:46. CrossRef
  11. Tomita K, Caramori G, Lim S, Ito K, Hanazawa T, Oates T, Chiselita I, Jazrawi E, Chung KF, Barnes PJ, Adcock IM: Increased p21(Cip1/Waf1) and B cell lymphoma leukemia-x(L) expression and reduced apoptosis in alveolar macrophages from smokers. / Am J Respir Crit Care Med 2002,166(5):724-31. CrossRef
  12. Miyazaki T, Hirokami Y, Matsuhashi N, Takatsuka H, Naito M: Increased susceptibility of thymocytes to apoptosis in mice lacking AIM, a novel murine macrophage-derived soluble factor belonging to the scavenger receptor cysteine-rich domain superfamily. / J Exp Med 1999,189(2):413-22. CrossRef
  13. Arai S, Shelton JM, Chen M, Bradley MN, Castrillo A, Bookout AL, Mak PA, Edwards PA, Mangelsdorf DJ, Tontonoz P, Miyazaki T: A role for the apoptosis inhibitory factor Aim/Spalpha/Api6 in atherosclerosis development. / Cell Metab 2005,1(3):201-13. CrossRef
  14. Kuwata K, Watanabe H, Jiang SY, Yamamoto T, Tomiyama-Miyaji C, Abo T, Miyazaki T, Naito M: Aim inhibits apoptosis of T cells and NKT cells in corynebacterium-induced granuloma formation in mice. / Am J Pathol 2003,162(3):837-47. CrossRef
  15. Araya J, Cambier S, Markovics JA, Wolters P, Jablons D, Hill A, Finkbeiner W, Jones K, Broaddus VC, Sheppard D, Barzcak A, Xiao Y, Erle DJ, Nishimura SL: Squamous metaplasia amplifies pathologic epithelial-mesenchymal interactions in COPD patients. / J Clin Invest 2007,117(11):3551-562. CrossRef
  16. Araya J, Maruyama M, Inoue A, Fujita T, Kawahara J, Sassa K, Hayashi R, Kawagishi Y, Yamashita N, Sugiyama E, Kobayashi M: Inhibition of proteasome activity is involved in cobalt-induced apoptosis of human alveolar macrophages. / Am J Physiol Lung Cell Mol Physiol 2002,283(4):L849-58.
  17. Fujii S, Hara H, Araya J, Takasaka N, Kojima J, Ito S, Minagawa S, Yumino Y, Ishikawa T, Numata T, Kawaishi M, Hirano J, Odaka M, Morikawa T, Nishimura S, Nakayama K, Kuwano K: Insufficient autophagy promotes bronchial epithelial cell senescence in chronic obstructive pulmonary disease. / OncoImmunology 2012,1(5):630-41. CrossRef
  18. Numata T, Araya J, Fujii S, Hara H, Takasaka N, Kojima J, Minagawa S, Yumino Y, Kawaishi M, Hirano J, Odaka M, Morikawa T, Nishimura SL, Nakayama K, Kuwano K: Insulin-dependent phosphatidylinositol 3-kinase/Akt and ERK signaling pathways inhibit TLR3-mediated human bronchial epithelial cell apoptosis. / J Immunol 2011,187(1):510-19. CrossRef
  19. Hu W, Xie J, Zhao J, Xu Y, Yang S, Ni W: Involvement of Bcl-2 family in apoptosis and signal pathways induced by cigarette smoke extract in the human airway smooth muscle cells. / DNA Cell Biol 2009,28(1):13-2. CrossRef
  20. Shaykhiev R, Krause A, Salit J, Strulovici-Barel Y, Harvey BG, O’Connor TP, Crystal RG: Smoking-dependent reprogramming of alveolar macrophage polarization: implication for pathogenesis of chronic obstructive pulmonary disease. / J Immunol 2009,183(4):2867-883. CrossRef
  21. Byers DE, Holtzman MJ: Alternatively activated macrophages and airway disease. / Chest 2011,140(3):768-74. CrossRef
  22. Barnes PJ: The cytokine network in chronic obstructive pulmonary disease. / Am J Respir Cell Mol Biol 2009,41(6):631-38. CrossRef
  23. Hodge S, Matthews G, Mukaro V, Ahern J, Shivam A, Hodge G, Holmes M, Jersmann H, Reynolds PN: Cigarette smoke-induced changes to alveolar macrophage phenotype and function are improved by treatment with procysteine. / Am J Respir Cell Mol Biol 2011,44(5):673-81. CrossRef
  24. Sipahi EY, Ozel Tekin I, Comert M, Barut F, Ustun H, Sipahi TH: Oxidized low-density lipoproteins accumulate in rat lung after experimental lung edema induced by alpha- naphthylthiourea (ANTU). / Pharmacol Res 2004,50(6):585-91. CrossRef
  25. Zhou J, Ryan AJ, Medh J, Mallampalli RK: Oxidized lipoproteins inhibit surfactant phosphatidylcholine synthesis via calpain-mediated cleavage of CTP: Phosphocholine cytidylyltransferase. / J Biol Chem 2003,278(39):37032-7040. CrossRef
  26. Heguy A, O’Connor TP, Luettich K, Worgall S, Cieciuch A, Harvey BG, Hackett NR, Crystal RG: Gene expression profiling of human alveolar macrophages of phenotypically normal smokers and nonsmokers reveals a previously unrecognized subset of genes modulated by cigarette smoking. / J Mol Med (Berl) 2006,84(4):318-28. CrossRef
  27. Ohar JA, Hamilton RF Jr, Zheng S, Sadeghnejad A, Sterling DA, Xu J, Meyers DA, Bleecker ER, Holian A: COPD is associated with a macrophage scavenger receptor-1 gene sequence variation. / Chest 2010,137(5):1098-107. CrossRef
  28. Kurokawa J, Arai S, Nakashima K, Nagano H, Nishijima A, Miyata K, Ose R, Mori M, Kubota N, Kadowaki T, Oike Y, Koga H, Febbraio M, Iwanaga T, Miyazaki T: Macrophage-derived AIM is endocytosed into adipocytes and decreases lipid droplets via inhibition of fatty acid synthase activity. / Cell Metab 2010,11(6):479-92. CrossRef
  29. van den Borst B, Gosker HR, Wesseling G, de Jager W, Hellwig VA, Snepvangers FJ, Schols AM: Low-grade adipose tissue inflammation in patients with mild-to-moderate chronic obstructive pulmonary disease. / Am J Clin Nutr 2011,94(6):1504-512. CrossRef
  
• 作者单位：Jun Kojima (1)
  Jun Araya (1)
  Hiromichi Hara (1)
  Saburo Ito (1)
  Naoki Takasaka (1)
  Kenji Kobayashi (1)
  Satoko Fujii (1)
  Chikako Tsurushige (1)
  Takanori Numata (1)
  Takeo Ishikawa (1)
  Kenichiro Shimizu (1)
  Makoto Kawaishi (1)
  Keisuke Saito (1)
  Noriki Kamiya (2)
  Jun Hirano (2)
  Makoto Odaka (2)
  Toshiaki Morikawa (2)
  Hiroshi Hano (3)
  Satoko Arai (4)
  Toru Miyazaki (4)
  Yumi Kaneko (1)
  Katsutoshi Nakayama (1)
  Kazuyoshi Kuwano (1)
  
  1. Department of Internal Medicine, Division of Respiratory Diseases, Jikei University School of Medicine, 3-25-8 Nishi-shimbashi, Minato-ku, Tokyo, 105-8461, Japan
  2. Department of Surgery, Division of Chest Diseases, Jikei University School of Medicine, Tokyo, Japan
  3. Department of Pathology, Jikei University School of Medicine, Tokyo, Japan
  4. Laboratory of Molecular Biomedicine for Pathogenesis, Center for Disease Biology and Integrative Medicine, Faculty of Medicine, The University of Tokyo, Tokyo, Japan
  

文摘

Background Marked accumulation of alveolar macrophages (AM) conferred by apoptosis resistance has been implicated in pathogenesis of chronic obstructive pulmonary disease (COPD). Apoptosis inhibitor of macrophage (AIM), has been shown to be produced by mature tissue macrophages and AIM demonstrates anti-apoptotic property against multiple apoptosis-inducing stimuli. Accordingly, we attempt to determine if AIM is expressed in AM and whether AIM is involved in the regulation of apoptosis in the setting of cigarette smoke extract (CSE) exposure. Methods Immunohistochemical evaluations of AIM were performed. Immunostaining was assessed by counting total and positively staining AM numbers in each case (n-- in control, n-- in non-COPD smoker, n-- in COPD). AM were isolated from bronchoalveolar lavage fluid (BALF). The changes of AIM expression levels in response to CSE exposure in AM were evaluated. Knock-down of anti-apoptotic Bcl-xL was mediated by siRNA transfection. U937 monocyte-macrophage cell line was used to explore the anti-apoptotic properties of AIM. Results The numbers of AM and AIM-positive AM were significantly increased in COPD lungs. AIM expression was demonstrated at both mRNA and protein levels in isolated AM, which was enhanced in response to CSE exposure. AIM significantly increased Bcl-xL expression levels in AM and Bcl-xL was involved in a part of anti-apoptotic mechanisms of AIM in U937 cells in the setting of CSE exposure. Conclusions These results suggest that AIM expression in association with cigarette smoking may be involved in accumulation of AM in COPD.