新生儿Fc受体在人肾小球肾炎及大鼠肾炎模型中的表达
Expression of neonatal Fc receptor on human nephritis and rat nephritis models
摘要目的 观察人肾小球肾炎及大鼠肾炎动物模型中,足细胞新生儿Fc受体(FcRn)的表达.方法 (1)收集2009年9月至2010年2月复旦大学医学院病理学系人肾穿刺组织标本39例(包括微小病变病8例、局灶节段性肾小球硬化症4例、IgA肾病12例、膜性肾病9例、狼疮性肾炎6例).透明细胞癌癌旁肾组织5例用作正常对照组.激光捕获显微切割技术分离肾小球,即时逆转录聚合酶链反应(RT-PCR)检测FcRn的mRNA水平,行免疫组织化学(Supervision法)染色观察FcRn在肾小球内表达的定位和强度差异.(2)构建大鼠系膜增生性肾炎(抗Thy1.1肾炎)和大鼠被动型膜性肾病(Heymann肾炎)模型,免疫组织化学(Supervision法)检测FcRn在肾组织内的表达.结果 人肾活检组织中,即时定量RT-PCR显示狼疮性肾炎的FcRn mRNA水平显著高于正常肾组织(P<0.05);免疫组织化学结果显示人各型肾炎中FcRn表达阳性率为:狼疮性肾炎6/6,IgA肾病7/12,膜性肾病6/9,均明显高于正常肾组织(0/5,P<0.05);微小病变病(1/8)、局灶节段性肾小球硬化症(0/4)与正常组相比差异无统计学意义(P>0.05).大鼠肾炎模型中,5例抗Thy1.1肾炎中3例、7例Heymann肾炎中2例可见足细胞表达FcRn,5例正常对照中,FcRn均不表达.结论 在免疫复合物介导的人肾小球肾炎和大鼠肾炎模型中,肾小球足细胞FcRn表达上调,FcRn的表达改变可能参与了肾小球肾炎的发生发展.
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abstractsObjective To study the expression of neonatal Fc receptor in podocytes in human nephritis and immune-induced rat nephritis models:anti-Thy1.1 nephritis and Heymann nephritis.Methods Thirty-nine cases of renal biopsies were enrolled from September 2009 to February 2010,including 8 cases of minimal change disease, 4 cases of focal segmental glomerulosclerosis, 9 cases of membranous nephropathy,12 cases of IgA nephropathy and 6 cases of lupus nephritis.Five normal kidney tissue samples adjacent to renal clear-cell carcinoma were served as normal controls.Laser capture microdissection and realtime RT-PCR were used to assess the expression level of FcRn mRNA in glomeruli of various glomerulonephritides,and immunohistochemistry (IHC) of FcRn by SuperVision method was performed.In addition,rat models of mesangial proliferative nephritis (anti-Thyl.1 nephritis) and passive membranous nephropathy (Heymann nephritis ) were established and FcRn was examined in renal tissues by IHC.Results The FcRn mRNA level in lupus nephritis was statistically higher than that of normal controls ( P < 0.05 ).FcRn protein expression by IHC was seen in lupus nephritis (6/6),membranous nephropathy (6/9) and IgA nephropathy (7/12),significantly higher than that of normal controls (0/5),P < 0.05.Minimal change disease and focal segmental glomerular sclerosis showed minimal or none expression of FcRn (1/8,0/4 respectively) and not statistically difference from that of normal controls. Furthermore,FcRn expression in podocytes was detected in rat anti-Thy1.1 (3/5) and Heymann nephritis models (2/7) but was not detected in normal controls. Conclusions Expression of FcRn in podocytes was up-regulated in immune-induced human nephritis and rat nephritis models of anti-Thyl.1 nephritis and Heymann nephritis.FcRn may play a role in the development of immune-induced glomerulonephritis.
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