The status and progress of relationship between macrophages polarization and choroidal neovascularization_Chinese Journal of Ocular Fundus Diseases

Authors：

ZhangPengfei ,  SunXiaodong

Department of Ophthalmology, The First People's Hospital Affiliated to Shanghai JiaoTong University, Shanghai 200080, China;

Corresponding author：

SunXiaodong, Email: xdsun@sjtu.edu.cn

Keywords：

Choroidal neovascularization/etiology; Macrophages; Review

DOI：

10.3760/cma.j.issn.1005-1015.2016.01.027

Video：

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Macrophages are major effecter cells of nonspecific immune response, the polarization of which plays a great role in inflammation, repairing and angiogenesis. According to functional phenotypes, macrophages can be polarized to classically activated type (M1), which could promote angiogenesis, and alternatively activated type (M2), which could inhibit angiogenesis. The proportion of M1/M2 could modulate the growth of choroidal neovascularization (CNV). Under the conditions of aging and injury within the retina, macrophages may polarize to M2, which could generate several proangiogenic factors, initiating and promoting the formation of angiogenesis and fibrous scar. Therefore, regulation of macrophage polarization is expected to inhibit angiogenesis and provide new insight for treatment of CNV.

Citation： ZhangPengfei, SunXiaodong. The status and progress of relationship between macrophages polarization and choroidal neovascularization. Chinese Journal of Ocular Fundus Diseases, 2016, 32(1): 96-99. doi: 10.3760/cma.j.issn.1005-1015.2016.01.027 Copy

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1. Lim LS, Mitchell P, Seddon JM, et al. Age-related macular degeneration[J]. Lancet, 2012,379(9827): 1728-1738. DOI: 10.1016/S0140-6736(12)60282-7.
2. Apte RS. Regulation of angiogenesis by macrophages[J].Adv Exp Med Biol, 2010, 664: 15-19.DOI: 10.1007/978-1-4419-1399-9_2.
3. Mantovani A, Sica A. Macrophages, innate immunity and cancer:balance, tolerance, and diversity[J]. Curr Opin Immunol, 2010, 22(2):231-237.DOI: 10.1016/j.coi.2010.01.009.
4. 雷蕾, 丁小燕, 唐仕波.巨噬细胞与小胶质细胞在老年性黄斑变性发病机制中的调控作用[J].中华眼底病杂志, 2010, 26(6): 588-591.DOI:10.3760/cma.j.issn.1005-1015.2010.06.33.Lei L, Ding XY, Tang SB. The regulation effects of macrophage and microglial cell in the pathogenesis of age-related macular degeneration[J]. Chin J Ocul Fundus Dis, 2010, 26(6): 588-591.DOI:10.3760/cma.j.issn.1005-1015.2010.06.33.
5. Biswas SK,Chittezhath M,Shalova IN,et al. Macrophage polarization and plasticity in health and disease[J].Immunol Res, 2012, 53(1-3): 11-24.DOI: 10.1007/s12026-012-8291-9.
6. Mantovani A, Sica A, Sozzani S, et al.The chemokine system in diverse forms of macrophage activation and polarization[J]. Trends Immunol, 2004, 25(12): 677-686. DOI: http://dx.doi.org/10.1016/j.it.2004.09.015.
7. Medzhitov R. Origin and physiological roles of inflammation[J]. Nature, 2008, 454(7203):428-435. DOI: 10.1038/nature07201.
8. Sica A, Schioppa T, Mantovani A, et al. Tumour-associated macrophages are a distinct M2 polarised population promoting tumour progression: potential targets of anticancer therapy[J]. Eur J Cancer, 2006, 42: 717-727.
9. Ma J, Mehta M, Lam G, et al. Influence of subretinal fluid in advanced stage retinopathy of prematurity on proangiogenic response and cell proliferation[J]. Mol Vis, 2014, 20: 881-893.
10. Kim J, Kim DW, Ha Y et al. Wnt5a induces endothelial inflammation via beta-catenin-independentsignaling[J].Immunol, 2010,185:1274-1282. DOI:4049/jimmunol.1000181.
11. Cao XG, Shen DF, Patel MM,et al. Macrophage polarization in the maculae of age-related macular degeneration: a pilot study[J]. Pathol Int, 2011, 61(9): 528-535. DOI: 10.1111/j.1440-1827.2011.02695.x.
12. Zhao H, Roychoudhury J, Doggett TA, et al.Age-dependent changes in FasL (CD95L) modulate macrophage function in a model of age-related macular degeneration[J]. Invest Ophthalmol Vis Sci, 2013, 54(8):5321-5331. DOI: 10.1167/iovs.13-12122.
13. Kelly J, Ali Khan A, Yin J, et al. Senescence regulates macrophage activationand angiogenic fate at sites of tissue injury in mice[J]. J Clin Invest, 2007,117(11):3421-3426. DOI: 10.1172/JCI32430.
14. McMenamin PG.Macrophages coming of age:their role in promoting CNV is modulated by FasL[J]. Invest Ophthalmol Vis Sci, 2013, 54(8):5332. DOI: 10.1167/iovs.13-12718.
15. Liu J, Copland DA, Horie S, et al.Myeloid cells expressing VEGF and arginase-1 followinguptake of damaged retinal pigment epithelium suggests potential mechanism that drives the onset of choroidal angiogenesis in mice[J/OL]. PLoS One, 2013, 8(8):72935[2013-08-16].http://dx.plos.org/10.1371/journal.pone.0072935.DOI:10.1371/journal.pone.0072935.
16. Horie S, Robbie SJ, Liu J, et al.CD200R signaling inhibits pro-angiogenic gene expression by macrophages and suppresses choroidal neovascularization[J].Sci Rep, 2013,3:3072. DOI: 10.1038/srep03072.
17. Daley JM, Brancato SK, Thomay AA, et al. The phenotype of murine wound macrophages[J]. J Leukoc Biol 2010, 87(1):59-67. DOI: 10.1189/jlb.0409236.
18. He LZ, Marneros AG. Macrophages are essential for the early wound healing response and the formation of a fibrovascular scar[J]. Am J Pathol, 2013,182(6): 2407-2417. DOI: 10.1016/j.ajpath.2013.02.032.
19. Espinosa-Heidmann DG,Suner IJ,Hernandez EP,et al. Macrophage depletion diminishes lesion size and severity in experimental choroidal neovascularization[J].Invest Ophthalmol Vis Sci, 2003, 44(8): 3586-3592.
20. Yamada K, Sakurai E, Haya M, et al.Inhibition of laser-induced choroidal neovascu1arization by atorvastatin by down regulation of monocyte chemotactic protein-1 synthesis in mice[J]. Invest Ophthalml Vis Sci, 2007, 48(4): 1839-1843.
21. Apte RS, Richter J, Herndon J, et al. Macrophages inhibit neovascularization in a murine model of age-related macular degeneration[J/OL]. PLoS Med, 2006, 3(8): 310[2006-08-03]. http://dx.plos.org/10.1371/journal.pmed.0030310. DOI: 10.1371/journal.pmed.0030310.
22. He L, Marneros AG. Doxycycline inhibits polarization of macrophages to the proangiogenic M2 type and subsequent neovascularization[J]. J Biol Chem, 2014, 289(12):8019-8028. DOI: 10.1074/jbc.M113.535765.
23. Coultas L, Chawengsaksophak K, Rossant J. Endothelial cells and VEGF in vascular development[J].Nature, 2005, 438(7070):937-945. DOI:10.1038/nature04479.
24. Carmi Y, Voronov E, Dotan S,et al. The role of macrophage-derived IL-1 in induction and maintenance of angiogenesis[J]. J Immunol, 2009,183(7):4705-4714. DOI: 10.4049/jimmunol.0901511.
25. Nagineni CN, Kommineni VK, William A, et al.Regulation of VEGF expression in human retinal cells by cytokines: implications for the role of inflammation in age-related macular degeneration[J].J Cell Physiol, 2012, 227(1):116-126. DOI: 10.1002/jcp.22708.
26. Marneros AG. NLRP3 inflammasome blockade inhibits VEGF-A-induced age-related macular degeneration[J]. Cell Rep,2013,4(5): 945-958. DOI: 10.1016/j.celrep.2013.08.002.
27. Xie P, Kamei M, Suzuki M, et al. Suppression and regression of choroidal neovascularization in mice by a novel CCR2 antagonist, INCB3344[J/OL]. PLoS One, 2011,6(12): 28933[2011-12-19]. http://dx.plos.org/10.1371/journal.pone.0028933. DOI: 10.1371/journal.pone.0028933.
28. Krause TA, Alex AF, Engel DR, et al.VEGF-production by CCR2-dependent macrophages contributes to laser-induced choroidal neovascularization[J/OL]. PLoS One, 2014, 9(4): 94313[2014-04-08]. http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0094313. DOI: 10.1371/journal.pone.0094313.
29. Oda T, Morkawa N, Saito Y, et al. Molecular cloning and characterization of a novel type of histamine receptor preferentially expressed in leukocytes[J]. J Biol Chem, 2000, 275(47): 36781-36786. DOI: 10.1074/jbc.M006480200.
30. Kaneko H, Ye F, Ijima R,et al.Histamine H4 receptor as a new therapeutic target for choroidal neovascularization in age-related macular degeneration[J]. Br J Pharmacol, 2014,171(15):3754-3763. DOI: 10.1111/bph.12737.
31. Hautamaki A, Kivioja J, Seitsonen S, et al.The IL-8, VEGF, and CFH polymorphisms and bevacizumab in age-related macular degeneration[J].Ophthalmology, 2014, 121(4): 973-973. DOI: 10.1016/j.ophtha.2013.11.035.
32. Wu WK, Llewellyn OP, Bates DO,et al.IL-10 regulation of macrophage VEGF production is dependent on macrophage polarisation and hypoxia[J]. Immunobiology, 2010,215(9-10):796-803. DOI: 10.1016/j.imbio.2010.05.025.

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