期刊文献+

IL-13对正常人表皮成纤维细胞炎症及纤维化相关基因表达的影响

The Study of Inflammatory and Fibrosis-related Genes Expression on Interleukin 13 Treated Normal Human Dermal Fibroblasts
下载PDF
导出
摘要 目的探讨IL-13对正常人表皮成纤维细胞(NHDF)炎症及纤维化相关基因的作用,从而进一步了解IL-13在皮肤纤维化过程中的病理机制。方法将不同浓度的IL-13(0.1ng/mL,1ng/mL,10ng/mL)加入到体外培养的NHDF,作用24h后,采用实时定量PCR(Real-TimePCR)方法 ,研究不同浓度IL-13刺激NHDF后CCL-2,IL-13ra1,IL-13ra2,CTGF和Pro-collagenI基因的表达情况。结果不同浓度的IL-13刺激NHDF24h后,CCL-2,IL-13ra2和Pro-collagenI基因表达显著增加(P<0.05),并呈剂量依赖关系;IL-13ra1和CTGF基因表达无明显改变(P>0.05)。结论 CCL-2,IL-13ra2和Pro-collagenI基因的高表达可能参与了IL-13在皮肤组织纤维化中的病理过程。 To investigate the effects of IL-13 on inflammatory and fbrosis-related genes expression in nordermal fibroblasts (NHDF). Methods To add different concentrations of IL-13 (0.1 ng/mL, lng/mL, 10ng/mL) into the in-vitro-cultured NHDF, after 24-hours stimulation, extracted RNA, and applied the Real-Time PCR to investigate the genes expression of CCL-2, IL-13ral, IL-13ra2, CTGF and Pro- collagen I in IL-13 treated NHDF. Results After 24-hours IL-13 stimulation in NHDF, the genes express- ing of CCL-2, IL-13ra2 and Pro-collagen I were significantly and dose-dependently increased ( P 〈 0.05 ), while the IL-13ral and CTGF genes expressing were not significantly increased (P 〉 0.05 ). Conclusion Our results indicate that, CCL-2, IL-13ra2 and Pro-collagen I genes over expressing may involved in IL-13 pathological role in skin fibrosis .
出处 《中国皮肤性病学杂志》 CAS 北大核心 2010年第6期499-501,共3页 The Chinese Journal of Dermatovenereology
基金 教育部留学回国人员启动基金
关键词 IL-13 正常人表皮成纤维细胞 皮肤纤维化 基因表达 IL-13 NHDF Skin Fibrosis Gene Expression
  • 相关文献

参考文献9

  • 1齐庆,郭庆,谭国珍,毛越苹,曾凡钦.5-氮杂-2-脱氧胞苷对系统性硬皮病皮损成纤维细胞胶原蛋白及相关抑制因子表达的影响[J].岭南皮肤性病科杂志,2009,16(2):79-82. 被引量:4
  • 2Lafyatis R,York M.Innate immunity and inflammation in systemic sclerosis[J].Curt Opin Rheumato,2009,21(6):617-622.
  • 3李晶冰,崔盘根.与系统性硬皮病相关的细胞因子[J].国外医学(皮肤性病学分册),2005,31(4):235-237. 被引量:2
  • 4Granel B,Allanore Y,Chevillard C,et al.IL13RA2 gene polymor-phisms are associated with systemic sclerosis[J].J Rheumatol,2006,33(10):2015-2019.
  • 5Granel B,Chevillard C,Dessein A.Interleukin 13 and interleukin 13 receptor involvement in systemic sclerosis[J].Bev Med Interne,2007,28(9):613-622.
  • 6Antonelli A,Ferri C,Fallahi P,et al.CXCL10(alpha)and CCL2 (beta) chemokines in systemic sclerosis-a longitudinal study[J].Rheumatolegy,2008,47(1):45-49.
  • 7Chin BY,Mohsenin A,Li SX,et al.Stimulation of pro-1(I) collagen by TGF-1 in mesangial cells:role of the p38 MAPK pathway[J].Am J Physiol Renal Physiol,2001,280(3):495-504.
  • 8Gourh P,Mayes MD,Arnett FC.CTGF polymorphism associated with systemic sclerosis[J].N Engl J Med,2008,358(3):308-309.
  • 9Fonseca C,Lindahl GE,Ponticos M,et al.A polymorphism in the CT-GF promoter region associated with systemic sclerosis[J].N Engl J Med,2007,357(12):1210-1220.

二级参考文献27

  • 1Qi Q, Guo Q, Tan G, et al. Predictors of the scleroderma phenotype in fibroblasts from systemic sclerosis patients [ J ]. J Eur Acad Dermatol Venereol, 2009,23 (2) : 160 - 168.
  • 2Varga J, Abraham D. Systemic sclerosis: a prototypic muhisystem fibrotic disorder [ J ]. J Clin Invest, 2007, 117(3) :557 -567.
  • 3Strickland FM, Richardson BC. Epigenetics in autoimmunity- DNA methylation in systemic lupus erythematosus and beyond[J]. Autoimmunity, 2008,41 (4) :278 - 286.
  • 4Wang Y, Fan PS, Kahaleh B. Association between enhanced type I collagen expression and epigenetic repression of the FLI1 gene in scleroderma fibroblasts [ J]. Arthritis Rheum, 2006,54 ( 7 ) : 2271 - 2279.
  • 5Klose R J, Bird AP. Genomic DNA methylation: the mark and its mediators [ J ]. Trends Biochem Sci, 2006, 31(2) :89 -97.
  • 6Sapadin AN, Fleischmajer R. Treatment of scleroderma [J]. Arch Dermatol, 2002,138( 1 ) :99 - 105.
  • 7Christman JK. 5 - Azacytidine and 5 - aza - 2' - deoxycytidine as inhibitors of DNA methylation: mechanistic studies and their implications for cancer therapy[J]. Oncogene, 2002,21 ( 35 ) :5483 - 5495.
  • 8Denton CP, Abraham DJ. Transforming growth factor-beta and connective tissue growth factor: key cytokines in scleroderma pathogenesis. Curr Opin Rheumatol, 2001,13:505-511.
  • 9Kawakami T, Ihn H, Xu W, et al. Increased expression of TGF-beta receptors by scleroderma fibroblasts: evidence for contribution of autocrine TGF-beta signaling to scleroderma phenotype. J Invest Dermatol, I998,110:47-51.
  • 10Kikuchi K, Kadono T, Ihn H, et al. Growth regulation in scleroderma fibroblasts: increased response to transforming growth factor-beta I. J Invest Dermatol, 1995,105:128-132.

共引文献4

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部