期刊文献+

不同类型白癜风基因谱表达差异的初步研究 被引量:3

Preliminary study of differential gene expression profiling between segmental vitiligo and non-segmental vitiligo
在线阅读 下载PDF
导出
摘要 目的探讨白癜风临床类型与基因表达差异的相关性。方法分别选择节段型白癜风(SV)、非节段型白癜风(NSV)和健康对照(HI)各4例,应用Phalanx人全基因组表达谱芯片检测外周血淋巴细胞基因谱表达差异,并通过RTPCR进行验证。结果与HI相比,SV有239个上调基因和175个下调基因,主要涉及适应性免疫反应、细胞因子受体相互作用、趋化因子信号通路,NSV有88个上调基因和560个下调基因,涉及先天性免疫、细胞自噬与凋亡、黑素细胞生物学、泛素介导的蛋白裂解与酪氨酸酶代谢。SV和NSV共同基因表达差异包括60个上调基因和60个下调基因;相对于SV,NSV表达223个上调基因和129个下调基因,主要包括嘌呤、嘧啶、鞘脂类代谢。结论 SV有不同于NSV的遗传背景与发病机制。 Objective To investigate the correlation between clinical pattern and differential gene expression in pa- tients with vitiligo. Methods Peripheral blood lymphoeytes obtained from four cases of segmental vitiligo (SV), non-segmental vitiligo (NSV) and healthy individual (HI) respectively. Whole genome expression microarrays were used to assay the gene expression profiles between SV, NSV and HI. Quantitative PCR assay was used to vali- date the gene expression of array. Results Compared to HI, 239 over-expressed and 175 down-expressed genes were detected in SV, which were mainly involved in the adaptive immune response, cytokine-cytokine receptor in- teraction and chemokine signaling. In NSV, 88 over-expressed and 560 down-expressed genes were found and were mainly involved in the innate immune, autophagy, apoptosis, melanocyte biology, ubiquitin mediated proteolysis and tyrosine metabolism, which were different from SV. Sixty over-expressed and sixty down-expressed genes shared similar tendency in SV and NSV. Compared to SV, 223 over-regulated and 129 down-regulated genes were found in NSV, which were mainly involved in the metabolism of purine, pyrimidine and sphingolipid. Conclusion There may exit different genetic background and pathogenesis between SV and NSV.
出处 《安徽医科大学学报》 CAS 北大核心 2016年第5期707-711,共5页 Acta Universitatis Medicinalis Anhui
基金 杭州市医学重点专科专病项目(编号:20140733Q19) 浙江省医药卫生科技计划项目(编号:2014KYB200)
关键词 白癜风 节段型 白癜风 非节段型 基因表达 segmental vitiligo non-segmental vitiligo gene expression
  • 相关文献

参考文献11

  • 1Passeron T, Ortonne J P. Physiopathology and genetics of vitiligo [ J]. J Autoimrnun,2005,25:63 - 8.
  • 2Guerra L, Dellambra E, Brescia S, et al. Vitiligo : pathogenetic hy- potheses and targets for current therapies [ J ]. Curr Drug Metab, 2010,11(5) :451 -67.
  • 3王平,洪为松,章莉,洪健,郑俊惠,许爱娥.白癜风表皮黑素细胞超微结构及小眼畸形相关转录因子转录调控研究[J].中华皮肤科杂志,2010,43(7):485-488. 被引量:5
  • 4倪亚杰,王平,洪为松,章莉,郑俊惠.小眼畸形相关转录因子转录调控与白癜风临床类型的相关性研究[J].医学研究杂志,2013,42(3):52-55. 被引量:2
  • 5Le Poole I C, Luiten R M. Autoimmune etiology of generalized viti- ligo [ J ]. Curr Dir Autoimmun ,2008,10:227 - 43.
  • 6Jeong T J, Shin M K, Uhm Y K, et al. Association of UVRAG polymorphisms with susceptibility to non-segmental vitiligo in a Ko- rean sample [ J ]. Exp Dermato1,2010,19 ( 8 ) : e323 - 5.
  • 7Glassman S J. Vitiligo, reactive oxygen species and T-cells [ J ]. Clin Sci (Lond) ,2011,120 ( 3 ) :99 - 120.
  • 8Dell' Anna M L, Maresca Y, Briganti S, et al. Mitoehondrial im- pairment in peripheral blood mononuclear cells during the active phase of vitiligo [ J ]. J Invest Dermato1,2001,117 (4) :908 - 13.
  • 9Moretti S, Fabbri P, Baroni G,et,al. Keratinocyte dysfunction in vitiligo epidermis:cytokine micmenvironment and correlation toke- ratinocyte apoptosis [ J 1. HistolHistopathol, 2009,24 ( 7 ) : 849 - 57.
  • 10Lee A Y, Youm Y H, Kim N H. Keratinocytes in the depigmented epidermis of vitiligo are more vulnerable to trauma (suction) than kcratinocytes in the normally pigmented epidermis, resulting in their apoptosis [ J ]. Br J Dermato1,2004,151 ( 5 ) : 995 - 1003.

二级参考文献24

  • 1Gauthier Y,Cario Andre M,Taieb A.A critical appraisal of vitiligo etiologic theories.Is melanocyte loss a melanocytorrhagy? Pigment Cell Res,2003,16(4):322-332.
  • 2Dell'anna ML,Pieardo M.A review and a new hypothesis for non-immunological pathogenetic mechanisms in vitiligo.Pigment Cell Res,2006,19(5):406-411.
  • 3Steingímsson E,Copeland NG,Jenkins NA.Melanocytes and the microphthalmia transcription factor network.Annu Rev Genet,2004.38:365-411.
  • 4Yamaguchi Y,Hearing VJ.Physiological factors that regulate skin pigmentation.Biofactors,2009,35(2):193-199.
  • 5Prignano F,Pescitclli L,Becatti M,et al.Ultrastructural and functional alterations of mitochondria in perilesional vitiligo skin.J Dermatol Sci,2009,54(3):157-167.
  • 6Panuncio AL,Vignale R.Ultrastructural studies in stable vitiligo.Am J Dermatopathol,2003,25(1):16-20.
  • 7Bartosik J,Wulf HC,Kobayasi T.Melanin and melanosome complexes in long standing stable vitiligo-an ultrastructural study.Eur J Dermatol,1998,8(2):95-97.
  • 8Tobin DJ,Swanson NN,Pittelkow MR,et al.Melanocytes are not absent in lesional skin of long duration vitiligo.J Pathol,2000,191(4):407-416.
  • 9Tassabehji M,Newton VE,Read AP.Waardenburg syndrome type.2 caused by mutations in the human micmphthalmia (MITF) gene.Nat Genet,1994,8(3):251-255.
  • 10Kurita K,Nishito M,Shimogaki H,et al.Suppression of progressive loss of coat color in microphthalmia-vitiligo mutant mice.J Invest Dermatol,2005,125(3):538-544.

共引文献5

同被引文献16

引证文献3

二级引证文献1

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