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Research Article

白细胞介素38在炎症诱导的角膜新生血管形成中的作用

卷 19, 期 8, 2019

页: [589 - 596] 页: 8

弟呕挨: 10.2174/1566524019666190627122655

价格: $65

摘要

背景：血管生成与炎症紧密相关。 白介素1（IL-1）家族的细胞因子是调节炎症反应的关键介质。 方法：在这项研究中，我们检查了IL-1家族成员IL-38在介导炎症诱导的血管生成中的作用。 结果：结果表明，在碱诱导的角膜新生血管（CNV）小鼠模型中，向受损的角膜局部施用IL-38可以减弱血管生成。 进一步的研究表明，在用IL-38处理的角膜中，炎症细胞因子TNF-α，IL-6，IL-8和IL-1β的表达降低了。 此外，在体外通过IL-38处理降低了血管生成活性，包括人视网膜内皮细胞的增殖，迁移和管形成。 结论：数据表明IL-38调节炎症诱导的血管生成。

关键词: 血管生成，细胞因子，白介素，炎症，IL-38，新血管形成。

« Previous Next »
[1]
Epstein RJ, Stulting RD, Hendricks RL, Harris DM. Corneal neovascularization. Pathogenesis and inhibition. Cornea 1987; 6(4): 250-7.
[http://dx.doi.org/10.1097/00003226-198706040-00004] [PMID: 2446823]
[2]
Polverini P J. The pathophysiology of angiogenesis. Critical reviews in oral biology and medicine: An official publication of the American Association of Oral Biologists 1995; 6: 230-47.
[http://dx.doi.org/10.1177/10454411950060030501]
[3]
Karizbodagh MP, Rashidi B, Sahebkar A, Masoudifar A, Mirzaei H. Implantation Window and Angiogenesis. J Cell Biochem 2017; 118(12): 4141-51.
[http://dx.doi.org/10.1002/jcb.26088] [PMID: 28436055]
[4]
Mashreghi M, Azarpara H, Bazaz MR, et al. Angiogenesis biomarkers and their targeting ligands as potential targets for tumor angiogenesis. J Cell Physiol 2018; 233(4): 2949-65.
[http://dx.doi.org/10.1002/jcp.26049] [PMID: 28608549]
[5]
Folkman J. Angiogenesis: An organizing principle for drug discovery? Nat Rev Drug Discov 2007; 6(4): 273-86.
[http://dx.doi.org/10.1038/nrd2115] [PMID: 17396134]
[6]
Jang YJ, Kim DS, Jeon OH, Kim DS. Saxatilin suppresses tumor-induced angiogenesis by regulating VEGF expression in NCI-H460 human lung cancer cells. J Biochem Mol Biol 2007; 40(3): 439-43.
[PMID: 17562297]
[7]
Biswas PS, Rouse BT. Early events in HSV keratitis--setting the stage for a blinding disease. Microbes Infect 2005; 7(4): 799-810.
[http://dx.doi.org/10.1016/j.micinf.2005.03.003] [PMID: 15857807]
[8]
Lee P, Wang CC, Adamis AP. Ocular neovascularization: an epidemiologic review. Surv Ophthalmol 1998; 43(3): 245-69.
[http://dx.doi.org/10.1016/S0039-6257(98)00035-6] [PMID: 9862312]
[9]
Hashemi Goradel N, Ghiyami-Hour F, Jahangiri S, et al. Nanoparticles as new tools for inhibition of cancer angiogenesis. J Cell Physiol 2018; 233(4): 2902-10.
[http://dx.doi.org/10.1002/jcp.26029] [PMID: 28543172]
[10]
Rashidi B, Malekzadeh M, Goodarzi M, Masoudifar A, Mirzaei H. Green tea and its anti-angiogenesis effects. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 2017; 89: 949-56.
[http://dx.doi.org/10.1016/j.biopha.2017.01.161]
[11]
Mirzaei H, Ferns GA, Avan A, Mobarhan MG. Cytokines and MicroRNA in Coronary Artery Disease. Adv Clin Chem 2017; 82: 47-70.
[http://dx.doi.org/10.1016/bs.acc.2017.06.004] [PMID: 28939213]
[12]
Folkman J, D’Amore PA. Blood vessel formation: what is its molecular basis? Cell 1996; 87(7): 1153-5.
[http://dx.doi.org/10.1016/S0092-8674(00)81810-3] [PMID: 8980221]
[13]
Chung AS, Ferrara N. Developmental and pathological angiogenesis. Annu Rev Cell Dev Biol 2011; 27: 563-84.
[http://dx.doi.org/10.1146/annurev-cellbio-092910-154002] [PMID: 21756109]
[14]
Sholley MM, Ferguson GP, Seibel HR, Montour JL, Wilson JD. Mechanisms of neovascularization. Vascular sprouting can occur without proliferation of endothelial cells. Lab Invest 1984; 51(6): 624-34.
[PMID: 6209468]
[15]
Kamba T, McDonald DM. Mechanisms of adverse effects of anti-VEGF therapy for cancer. Br J Cancer 2007; 96(12): 1788-95.
[http://dx.doi.org/10.1038/sj.bjc.6603813] [PMID: 17519900]
[16]
Voronov E, Shouval DS, Krelin Y, et al. IL-1 is required for tumor invasiveness and angiogenesis. Proc Natl Acad Sci USA 2003; 100(5): 2645-50.
[http://dx.doi.org/10.1073/pnas.0437939100] [PMID: 12598651]
[17]
Matsuo Y, Sawai H, Ma J, et al. IL-1alpha secreted by colon cancer cells enhances angiogenesis: the relationship between IL-1alpha release and tumor cells’ potential for liver metastasis. J Surg Oncol 2009; 99(6): 361-7.
[http://dx.doi.org/10.1002/jso.21245] [PMID: 19204921]
[18]
Park CC, et al. Evidence of IL-18 as a novel angiogenic mediator. J Immunol 2001; 167: 1644-53.
[19]
Choi YS, Choi HJ, Min JK, et al. Interleukin-33 induces angiogenesis and vascular permeability through ST2/TRAF6-mediated endothelial nitric oxide production. Blood 2009; 114(14): 3117-26.
[http://dx.doi.org/10.1182/blood-2009-02-203372] [PMID: 19661270]
[20]
Lin H, Ho AS, Haley-Vicente D, et al. Cloning and characterization of IL-1HY2, a novel interleukin-1 family member. J Biol Chem 2001; 276(23): 20597-602.
[http://dx.doi.org/10.1074/jbc.M010095200] [PMID: 11278614]
[21]
Bensen JT, Dawson PA, Mychaleckyj JC, Bowden DW. Identification of a novel human cytokine gene in the interleukin gene cluster on chromosome 2q12-14. J Interfer Cytokine Res 2001; 21: 899-904.
[http://dx.doi.org/10.1089/107999001753289505]
[22]
Kumar S, McDonnell PC, Lehr R, et al. Identification and initial characterization of four novel members of the interleukin-1 family. J Biol Chem 2000; 275(14): 10308-14.
[http://dx.doi.org/10.1074/jbc.275.14.10308] [PMID: 10744718]
[23]
van de Veerdonk FL, Stoeckman AK, Wu G, et al. IL-38 binds to the IL-36 receptor and has biological effects on immune cells similar to IL-36 receptor antagonist. Proc Natl Acad Sci USA 2012; 109(8): 3001-5.
[http://dx.doi.org/10.1073/pnas.1121534109] [PMID: 22315422]
[24]
Rudloff I, Godsell J, Nold-Petry CA, et al. Brief Report: Interleukin-38 Exerts Antiinflammatory Functions and Is Associated With Disease Activity in Systemic Lupus Erythematosus. Arthritis Rheumatol 2015; 67(12): 3219-25.
[http://dx.doi.org/10.1002/art.39328] [PMID: 26314375]
[25]
Dehghan A, Dupuis J, Barbalic M, et al. Meta-analysis of genome-wide association studies in >80000 subjects identifies multiple loci for C-reactive protein levels. Circulation 2011; 123(7): 731-8.
[http://dx.doi.org/10.1161/CIRCULATIONAHA.110.948570] [PMID: 21300955]
[26]
Rahman P, Sun S, Peddle L, et al. Association between the interleukin-1 family gene cluster and psoriatic arthritis. Arthritis Rheum 2006; 54(7): 2321-5.
[http://dx.doi.org/10.1002/art.21928] [PMID: 16918024]
[27]
Chou CT, Timms AE, Wei JC, Tsai WC, Wordsworth BP, Brown MA. Replication of association of IL1 gene complex members with ankylosing spondylitis in Taiwanese Chinese. Ann Rheum Dis 2006; 65(8): 1106-9.
[http://dx.doi.org/10.1136/ard.2005.046847] [PMID: 16361275]
[28]
Guo ZS, Li C, Lin ZM, et al. Association of IL-1 gene complex members with ankylosing spondylitis in Chinese Han population. Int J Immunogenet 2010; 37(1): 33-7.
[http://dx.doi.org/10.1111/j.1744-313X.2009.00889.x] [PMID: 19930406]
[29]
Monnet D, Kadi A, Izac B, et al. Association between the IL-1 family gene cluster and spondyloarthritis. Ann Rheum Dis 2012; 71(6): 885-90.
[http://dx.doi.org/10.1136/annrheumdis-2011-200439] [PMID: 22312160]
[30]
Lea WI, Lee YH. The associations between interleukin-1 polymorphisms and susceptibility to ankylosing spondylitis: a meta-analysis. Joint, Bone, Spine. Revue du Rhumatisme 2012; 79: 370-4.
[http://dx.doi.org/10.1016/j.jbspin.2011.06.010]
[31]
Ciccia F, Accardo-Palumbo A, Alessandro R, et al. Interleukin-36α axis is modulated in patients with primary Sjögren’s syndrome. Clin Exp Immunol 2015; 181(2): 230-8.
[http://dx.doi.org/10.1111/cei.12644] [PMID: 25902739]
[32]
Liang CC, Park AY, Guan JL. In vitro scratch assay: a convenient and inexpensive method for analysis of cell migration in vitro. Nat Protoc 2007; 2(2): 329-33.
[http://dx.doi.org/10.1038/nprot.2007.30] [PMID: 17406593]
[33]
Lin CM, Chang H, Chen YH, Li SY, Wu IH, Chiu JH. Protective role of wogonin against lipopolysaccharide-induced angiogenesis via VEGFR-2, not VEGFR-1. Int Immunopharmacol 2006; 6(11): 1690-8.
[http://dx.doi.org/10.1016/j.intimp.2006.07.003] [PMID: 16979123]
[34]
Sachdev U, Cui X, Hong G, et al. High mobility group box 1 promotes endothelial cell angiogenic behavior in vitro and improves muscle perfusion in vivo in response to ischemic injury. J Vasc Surg 2012; 55(1): 180-91.
[http://dx.doi.org/10.1016/j.jvs.2011.07.072] [PMID: 21944908]
[35]
Carmeliet P, Jain RK. Molecular mechanisms and clinical applications of angiogenesis. Nature 2011; 473(7347): 298-307.
[http://dx.doi.org/10.1038/nature10144] [PMID: 21593862]
[36]
Folkman J. Angiogenesis-dependent diseases. Semin Oncol 2001; 28(6): 536-42.
[http://dx.doi.org/10.1016/S0093-7754(01)90021-1] [PMID: 11740806]
[37]
Folkman J. Fundamental concepts of the angiogenic process. Curr Mol Med 2003; 3(7): 643-51.
[http://dx.doi.org/10.2174/1566524033479465] [PMID: 14601638]
[38]
Amano K, Okigaki M, Adachi Y, et al. Mechanism for IL-1 beta-mediated neovascularization unmasked by IL-1 beta knock-out mice. J Mol Cell Cardiol 2004; 36(4): 469-80.
[http://dx.doi.org/10.1016/j.yjmcc.2004.01.006] [PMID: 15081307]
[39]
Coxon A, Bolon B, Estrada J, et al. Inhibition of interleukin-1 but not tumor necrosis factor suppresses neovascularization in rat models of corneal angiogenesis and adjuvant arthritis. Arthritis Rheum 2002; 46(10): 2604-12.
[http://dx.doi.org/10.1002/art.10546] [PMID: 12384918]
[40]
van de Veerdonk FL, de Graaf DM, Joosten LA, Dinarello CA. Biology of IL-38 and its role in disease. Immunol Rev 2018; 281(1): 191-6.
[http://dx.doi.org/10.1111/imr.12612] [PMID: 29247986]
[41]
Bassoy EY, Towne JE, Gabay C. Regulation and function of interleukin-36 cytokines. Immunol Rev 2018; 281(1): 169-78.
[http://dx.doi.org/10.1111/imr.12610] [PMID: 29247994]
[42]
Xu WD, Huang AF. Role of Interleukin-38 in Chronic Inflammatory Diseases: A Comprehensive Review. Front Immunol 2018; 9: 1462.
[http://dx.doi.org/10.3389/fimmu.2018.01462] [PMID: 29988385]
[43]
Zhang J, Zhao R, Chen J, et al. The Effect of Interleukin 38 on Angiogenesis in a Model of Oxygen-induced Retinopathy. Sci Rep 2017; 7(1): 2756.
[http://dx.doi.org/10.1038/s41598-017-03079-z] [PMID: 28584235]
[44]
Pan B, Shen J, Cao J, et al. Interleukin-17 promotes angiogenesis by stimulating VEGF production of cancer cells via the STAT3/GIV signaling pathway in non-small-cell lung cancer. Sci Rep 2015; 5: 16053.
[http://dx.doi.org/10.1038/srep16053] [PMID: 26524953]
[45]
Vigne S, Palmer G, Lamacchia C, et al. IL-36R ligands are potent regulators of dendritic and T cells. Blood 2011; 118(22): 5813-23.
[http://dx.doi.org/10.1182/blood-2011-05-356873] [PMID: 21860022]

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