Komatsuda Atsushi, Wakui Hideki, Iwamoto Keiko, Harada Manabu, Okumoto Yasuhide, Sawada Ken-ichi
Third Department of Internal Medicine, Akita University School of Medicine, Akita, Japan.
Am J Nephrol. 2008;28(4):539-47. doi: 10.1159/000114098. Epub 2008 Jan 25.
It is hypothesized that minimal change nephrotic syndrome (MCNS) is a consequence of immune cell dysfunction that may lead to release of glomerular permeability factors. However, the nature of such factors remains uncertain.
Using cDNA microarrays, we performed gene expression profiling of peripheral blood mononuclear cells (PBMC) from 2 MCNS patients during nephrosis and remission phases. To confirm the cDNA microarray results, we performed quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR) analyses in nephrosis and remission samples from 24 MCNS patients and 10 patients with membranous nephropathy (MN), and from 24 healthy subjects.
Out of 24,446 genes screened, 171 functionally known genes were up-regulated (at least 2-fold) in PBMC from MCNS patients during the nephrosis phase. 21 genes encoded proteins involved in signal transduction and cytokine response. For further examination, we selected two genes encoding provable secretory proteins, chemokine (C-C) ligand 13 (CCL13) and a novel galectin-related protein (HSPC159). The results of quantitative RT-PCR showed that expressions of CCL13 and HSPC159 mRNA in nephrosis PBMC samples were higher than those in remission samples from all 24 MCNS patients examined, while these mRNA expression patterns were variable among 10 MN patients. CCL13 and HSPC159 mRNA expressions in PBMC from MCNS patients in nephrosis were significantly higher than those in nephrotic MN patients and healthy controls.
We found that CCL13 and HSPC159 mRNA expressions in PBMC are up-regulated specifically in MCNS patients during the nephrosis phase. Further studies are necessary to clarify whether these expression changes are directly involved in the pathophysiologic processes of MCNS.
据推测,微小病变肾病(MCNS)是免疫细胞功能障碍的结果,这可能导致肾小球通透性因子的释放。然而,这些因子的性质仍不确定。
我们使用cDNA微阵列,对2例MCNS患者在肾病期和缓解期的外周血单个核细胞(PBMC)进行基因表达谱分析。为了证实cDNA微阵列结果,我们对24例MCNS患者、10例膜性肾病(MN)患者以及24例健康受试者的肾病期和缓解期样本进行了定量实时逆转录聚合酶链反应(RT-PCR)分析。
在筛选的24446个基因中,171个功能已知基因在MCNS患者肾病期的PBMC中上调(至少2倍)。21个基因编码参与信号转导和细胞因子反应的蛋白质。为进一步研究,我们选择了两个编码可证实的分泌蛋白的基因,趋化因子(C-C)配体13(CCL13)和一种新的半乳糖凝集素相关蛋白(HSPC159)。定量RT-PCR结果显示,在所有24例接受检查的MCNS患者中,肾病期PBMC样本中CCL13和HSPC159 mRNA的表达高于缓解期样本,而这两种mRNA的表达模式在10例MN患者中各不相同。MCNS患者肾病期PBMC中CCL13和HSPC159 mRNA的表达显著高于肾病性MN患者和健康对照。
我们发现,PBMC中CCL13和HSPC159 mRNA的表达在MCNS患者肾病期特异性上调。需要进一步研究以阐明这些表达变化是否直接参与MCNS的病理生理过程。