CAJ | 학술논문

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.
목적 관찰인신소구신염급대서신염동물모형중,족세포신생인Fc수체(FcRn)적표체.방법 (1)수집2009년9월지2010년2월복단대학의학원병이학계인신천자조직표본39례(포괄미소병변병8례、국조절단성신소구경화증4례、IgA신병12례、막성신병9례、랑창성신염6례).투명세포암암방신조직5례용작정상대조조.격광포획현미절할기술분리신소구,즉시역전록취합매련반응(RT-PCR)검측FcRn적mRNA수평,행면역조직화학(Supervision법)염색관찰FcRn재신소구내표체적정위화강도차이.(2)구건대서계막증생성신염(항Thy1.1신염)화대서피동형막성신병(Heymann신염)모형,면역조직화학(Supervision법)검측FcRn재신조직내적표체.결과 인신활검조직중,즉시정량RT-PCR현시랑창성신염적FcRn mRNA수평현저고우정상신조직(P＜0.05)；면역조직화학결과현시인각형신염중FcRn표체양성솔위:랑창성신염6/6,IgA신병7/12,막성신병6/9,균명현고우정상신조직(0/5,P＜0.05)；미소병변병(1/8)、국조절단성신소구경화증(0/4)여정상조상비차이무통계학의의(P＞0.05).대서신염모형중,5례항Thy1.1신염중3례、7례Heymann신염중2례가견족세포표체FcRn,5례정상대조중,FcRn균불표체.결론 재면역복합물개도적인신소구신염화대서신염모형중,신소구족세포FcRn표체상조,FcRn적표체개변가능삼여료신소구신염적발생발전.
Objective 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.