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多发性肌炎外周血白细胞中细胞因子信号转导蛋白抑制因子基因表达的初步研究 被引量:1

Preliminary Research on the Expression of Suppressor of Cytokine Signaling in Peripheral Blood Leukocytes of Polymyositis Patients
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摘要 目的研究活动期多发性肌炎患者外周血白细胞细胞因子信号转导蛋白抑制因子(SOCS)1、SOCS2、SOCS3和细胞因子诱导的含SH2区域蛋白1(CIS)与正常人表达的差异,探讨SOCS在多发性肌炎发病中可能的作用。方法 2011年6月-12月,采用实时荧光定量聚合酶链反应法检测了14例活动期多发性肌炎患者和14例正常人外周血白细胞中SOCS1、SOCS2、SOCS3和CIS1基因的相对表达量。结果与对照组相比,多发性肌炎症患者外周血白细胞基因SOCS 1~3表达明显降低(P值均<0.05),CIS1基因的表达较对照组明显升高(P<0.05),差异有统计学意义。结论 SOCS基因家族可能参与了多发性肌炎的发病,该蛋白分子家族的成员可能会成为多发性肌炎治疗的一种新的候选基因。 Objective To investigate the difference of expression of suppressor of cytokine signaling(SOCS)(SOCS1,SOCS2,SOCS3) and cytokine-inducible SH2 containing protein 1(CIS1) in peripheral blood between polymyositis(PM) patients and healthy controls,and explore the possible roles of SOCS in the pathogenesis of PM.Methods From June to December 2001,peripheral blood samples from patients with PM(n=14) were collected and blood samples from 14 healthy adults were used as control.All the patients enrolled in this study were at active course of PM.The expression of SOCS 1-3 and CIS1 mRNA in peripheral blood leukocyte(PBL) from PM patients and healthy controls were quantified by real-time PCR analysis.Results The mRNA levels of SOCS 1-3 in PBL of PM patients were significantly lower than those in the healthy controls(P〈0.05).In contrast,CIS1 expression was significantly higher in PBL of PM patients in comparison with its expression in the healthy controls(P〈0.05).Conclusions SOCS mRNA expression levels are profoundly altered in PM patients,and SOCS cytokines may play an important role in the pathogenesis of PM.SOCS family may be a new candidate gene in the therapy of PM.
出处 《华西医学》 CAS 2012年第4期481-484,共4页 West China Medical Journal
基金 国家自然科学基金(30830094 30972678)~~
关键词 细胞因子信号转导蛋白抑制因子 细胞因子诱导的含SH2区域蛋白 多发性肌炎 Suppressors of cytokine signaling; Cytokine-inducible SH2 containing protein; Polymyositis
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  • 1Lundberg IE. New possibilities to achieve increased understanding of disease mechanisms in idiopathic inflammatory myopathies[J]. Curr Opin Rheumatol, 2002, 14(6): 639-642.
  • 2Starr R, Willson TA, Viney EM, et al. A family of cytokine-inducible inhibitors of signalling[J]. Nature, 1997, 387(6636): 917-921.
  • 3Endo TA, Masuhara M, Yokouchi M, et al. A new protein containing an SH2 domain that inhibits JAK kinases[J]. Nature, 1997, 387(6636): 921-924.
  • 4Yoshimura A, Nishinakamura H, Matsumura Y, et al. Negative regulation of cytokine signaling and immune responses by SOCS proteins[J]. Arthritis Res Ther, 2005, 7(3): 100-110.
  • 5Alexander WS. Suppressors of cytokine signalling (SOCS) in the immune system[J]. Nat Rev Immunol, 2002, 2(6): 410-416.
  • 6Alexander WS, Hilton DJ. The role of suppressors of cytokine signaling (SOCS) proteins in regulation of the immune response[J]. Annu Rev Immunol, 2004, 22: 503-529.
  • 7Kubo M, Hanada T, Yoshimura A. Suppressors of cytokine signaling and immunity[J]. Nat Immunol, 2003, 4(12): 1169-1176.
  • 8Bohan A, Peter JB.Polymyositis and dermatomyositis (second of two parts) [J]. N Engl J Med, 1975, 292(8): 403-407.
  • 9Bohan A, Peter JB. Polymyositis and dermatomyositis (first of two parts) [J]. N Engl J Med, 1975, 292(7): 344-347.
  • 10Miller FW, Rider LG, Chung YL, et al. Proposed preliminary core set measures for disease outcome assessment in adult and juvenile idiopathic inflammatory myopathies[J]. Rheumatology (Oxford), 2001, 40(11): 1262-1273.

二级参考文献15

  • 1Fornoni A,Ijaz A,Tejada T,et al.Role of inflammation in diabetic nepnephropa-thy.Curr Diabetes Rev,2008,4(1):10-17.
  • 2Ichinose K,Kawasaki E,Eguchi K.Recent advancement of understanding pathogenesis of type diabetes and potential relevance to diabetic nephropathy.Am J Nephrol,2007,27(6):554-564.
  • 3Su WC,Kitagawa M,Xue N,et al.Activation of stat1 by mutant fibroblastgrowth-factor receptor in thanatophoric dysplasia type II dwarfism.Nature,1997,386(6622):288-292.
  • 4Naka T,Narazaki M,Hirata M,et al.Structure and function of a new STAT-induced STAT inhibitor.Nature,1997,387(6636):924-929.
  • 5Starr R,Wilson TA,Viney EM,et al.A family of cytokine-inducible inhibitors of signalling.Nature,1997,387(6636):917-921.
  • 6Cunter W,Ziyadeh FN.Molecular mechanisms of diabetic renal hypertrophy.Kidney Int,1999,56(2):393-398.
  • 7Hirono T,Ishihara K,Hibi M.Roles of STAT3 in mediating the cell growth,differentiation and survival signals relayed through the IL-6 family of cytokine receptors.Oncogene,2000,19(3):2548-2556.
  • 8Heinrich PC,Behrmann I,Muller-Newen G,et al.Interleukin-6-type cytokine signaling through the gp130/JAK/STAT pathway.Biochem J,1998,334(Pt2):297-314.
  • 9Levy DE,Darnell JE.STATs:transcriptional control and biological impact.Nat Rev Mol Cell Biol,2002,3(9):651-662.
  • 10Al-Douahji M,Brugarolas J,Brown PA,et al.The cyclin kinase inhibitorp 21WAF1/CIP1 is required for glomerular hypertrophy in experimental diabetic nephropathy.Kidney Int,1999,56(5):1691-1699.

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