肥大细胞在IgA肾病中的表达及致病机制

Mast Cells Participated in the Development of IgA Nephropathy Through Renin

目的通过肥大细胞在Ig A肾病及其合并肾功能不全患者肾组织的染色,并探讨其在疾病进程中的可能作用机制。方法选取正常组12例、Ig A肾病患者20例、Ig A肾病合并轻度肾功能不全患者8例,进行肾组织肥大细胞染色及计数。在IL-6或TNF-α刺激下,通过实时定量PCR及免疫印迹法检测培养的肥大细胞中肾素m RNA及蛋白的表达。结果与正常组相比,Ig A肾病组及Ig A肾病合并肾功能不全组肥大细胞计数梯度升高(P=0.000),肥大细胞主要分布于肾间质,特别是纤维化区域。肥大细胞计数与小管萎缩、间质纤维化、球性肾小球硬化等存在相关关系。正常培养的肥大细胞表达肾素m RNA及蛋白,在IL-6或TNF-α刺激下,肾素的表达较正常组明显增多,在24h内呈时间依赖(P=0.000)。结论肥大细胞浸润参与Ig A肾病的疾病过程。在致纤维细胞因子干预下,肥大细胞肾素表达上调,干预肥大细胞浸润可能是Ig A肾病患者治疗的新靶标。

Objective To observe the expression of mast cell in IgA nephropathy and explore the underlying pathogenesis mecha-nism.Methods Renal biopsies consist of control kidney （ n=12 ） , IgA nephropathy group （ n=20 ） and IgA nephropathy associated with renal insufficiency group （n=8） for a quantitative evaluation of the MCs infiltration.Cultured MCs were divided into three groups：the control group, IL-6 group and TNF-αgroup.Real-Time PCR and Western blot were performed to quantify the renin in three groups.Results In a panel of human renal biopsy specimens, MCs showed gradient rise in control group, IgAN groups and IgAN associ-ated with renal insufficiency group.MCs were localized to the renal interstitium, especially in fibrotic areas, and few MCs infiltrated in glomeruli or tubular lumina.Increased MC count was significantly correlated with tubular atrophy, IF, interstitial inflammation, global glomerulosclerosis.Mast cells could express renin mRNA and protein in control group.MCs in group IL-6 and TNF-αgroup signifi-cantly increased renin expression than that in control in time-dependent manners （ P=0.000） .Conclusion MCs may play a vital role in progressive IgAN, and renin expression in MCs may contribute to this process.