期刊文献+

TNFAIP3和TNIP1基因在寻常型银屑病中的表达及意义 被引量:3

Significance of TNFAIP3 and TNIP1 gene expression in psoriasis vulgaris
下载PDF
导出
摘要 目的检测轻度和中重度寻常型银屑病患者的皮肤中肿瘤坏死因子-α诱导蛋白质3(TNFAIP3)和TNFAIP3相互作用蛋白质1(TNIP1)mRNA表达。方法采用实时荧光定量PCR来检测20例寻常银屑病患者皮损和正常皮肤中TNFAIP3和TNIP1 mRNA表达。结果与正常皮肤相比,10例轻度银屑病患者皮损中出现TNFAIP3基因表达下调和TNIP1基因表达上调(P<0.05)。10例中重度银屑病患者的正常皮肤和皮损中,TNFAIP3和TNIP1 mRNA表达差异无统计学意义(P>0.05)。结论 TNFAIP3和TNIP1 mRNA表达异常可能在寻常性银屑病的早期发挥作用。 Objective To observe the expression of tumor necrosis factor alpha-induced protein 3 (TNFAIP3) and TNFAIP3 interacting protein 1 (TNIP1) mRNA in the skin of patients with various degrees of psoriasis vulgaris (PV). Methods The expression of TNFAIP3 and TNIP1 mRNA was detected by quantitative real-time PCR in the skin lesion and normal-appearing skin of 20 PV patients. Results Compared with the normal-appearing skin, expression of TNFAIP3 mRNA decreased, but that of TNIP1 mRNA increased in the skin lesions of 10 cases of mild PV (P〈0.05). However, no statistical difference was observed in TNFAIP3 and TNIP1 mRNA expression between skin lesion and normal-appearing skin in 10 cases of moderate to severe PV (P〉0.05). Conclusion The abnormal expression of TNFAIP3 and TNIP1 mRNAmay play a role in the early stage of mild PV.
出处 《广东医学院学报》 2012年第4期358-360,363,共4页 Journal of Guangdong Medical College
基金 深圳市科技计划项目研发资金资助(No.201102139) 第35批教育部"留学回国人员科研启动基金" 上海市浦江人才计划
关键词 银屑病 肿瘤坏死因子-α诱导蛋白质3(TNFAIP3) TNFAIP3相互作用蛋白质1(TNIP1) psoriasis; tumor necrosis factor alpha-induced protein 3 (TNFAIP3); TNFAIP3 interacting protein 1(TNIP1)
  • 相关文献

参考文献4

二级参考文献327

  • 1李琼英,陈柏坤,卓佳,张丽芳.尖锐湿疣组织中NF-κBp65和IκB-α蛋白的表达及意义[J].温州医学院学报,2006,36(3):204-206. 被引量:1
  • 2李明鸣,刘林嶓,马长路.NF-κB/P65,p-IκBα,IκKα在皮肤SCC和BCC中的表达和意义[J].中国美容医学,2006,15(12):1339-1341. 被引量:2
  • 3Chen F, Castranova V, Shi X, et al. New insights into the role of nuclear factor- KappaB, a ubiquitous trascription factor in the initiation of diseases. Clin Chem 1999;45:7- 17.
  • 4Tak PP, Firestein GS. NF - KappaB : a key role in inflammatory diseases. J Clin Invest 2001 ; 107:7 - 11.
  • 5Anest V, Hanson JL, Cogswell PC, et al. A nucleosonnal function for IkappaB kinase- alpha in NF- KappaB- dependent gene expression. Nature 2003 ;423 : 659 - 663.
  • 6Klement JF, Rice NR, Car BD, et al. IkappaB a deficiency results in a sustained NF- KappaB response and Severe wideapread dermatis in mice. Mol Cell Biol 1996; 16:2341- 2349.
  • 7Barton D, HogenEsch H, Weih F. Mice lacking the transcription factor RelB develop T cell- dependent skin lesions similaer to human atopic dermatitis. Eur J Immunol 2000; 30: 2323 - 2332.
  • 8Nakamura H, Aoki M, Tamai K, et al. Prevention and regression of atopic dermatitis by ointment containing decoy NF- κB oligodeoxynucleotides in NC/Nga atopic mouse model. Gene Therapy 2002;9:1221 - 1229.
  • 9Bardaro T, Falco G, Sparago A, et al. Two cases of misinterpretation of molecular results in incontinentia pigmenti, and a PCR- based method to discriminate NEMO/IKK gamma dene deletion. Human Mutation 2003;21:8 - 11.
  • 10Sourav G, Vinay T, Carla VII, et al. Essential role of tuberous sclerosis genes TSC1 and TSC2 in NF- kappaB aetivation and eell survival. Cancer Cell 20136;10:215 - 226.

共引文献145

同被引文献48

  • 1李玉林.病理学[M].7版.北京:人民卫生出版社,2008:1.
  • 2陈晋广,任小丽.银屑病角质形成细胞凋亡与Fas/FasL表达的关系[J].浙江临床医学,2007,9(11):1465-1466. 被引量:1
  • 3Arsenescu R, Bruno ME, Rogier EW, et al. Signature biomarkers in Crnhn disease:toward a molecular classification [ J ]. Mucosal Im- muno1,2008,1 : 399 - 41 I.
  • 4Honma K,Tsuzuki S, Nakagawa M,et al. TNFAIP3/A20 functions as a novel tumor suppressor gene in several subtypes of non - Hodgkin lymphomas [ J ]. Blood,2009,114 ( 12 ) :2467 - 2475.
  • 5Sou SN, Ilieva KM, Polizzi KM. Binding of human BiP to the ER stress transducers IREI and PERK requires ATP[ J]. Biuchem Bio- phys Res Commun, 2012,420 ( 2 ) :473 - 478.
  • 6Schroder M, Sutcliffe L. Consequences of stress in the secretary pathway ,the ER stress response and its role in the metabolic syn-drome [J]. Methods Mol Bio1,2010 ,648 :43 - 62.
  • 7Meares GP, Zmijewska AA, Jope RS. HSP105 interacts with GRP78 and GSK3 and promotes ER stress -induced caspase -3 activation [ J ]. Cell Signal, 2008,20 : 347 - 358.
  • 8Bianchi L,Farrace M C,Nini G,et al.Abnormal bcl-2 and"Tissue"transglutaminase expression in psoriatic skin[J].J Invest Dermatol,1994,103(6):829-833.
  • 9Madonna S,Scarponi C,Pallotta S,et al.Anti-apoptotic effects of sup-pressor of cytokine signaling 3 and 1 in psoriasis[J].Cell Death Dis,2012,28(3):334.
  • 10Takahashi H,Manabe A,Ishida-Yamamoto A,et al.Aberrant expression of apoptosis-related molecules in psoriatic epidermis[J].J Dermatol Sci,2002,28(3):187-197.

引证文献3

二级引证文献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