Detection of nuclear factor-κB in IgA nephropathy using southwestern histochemistry
Detection of nuclear factor-κB in IgA nephropathy using southwestern histochemistry
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DOI：
10.1016/s0272-6386(03)00411-6
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发表时间：
2003-07-01
影响因子：
13.2
通讯作者：
Kohno, S
中科院分区：
文献类型：
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作者：
Ashizawa, M;Miyazaki, M;Kohno, S
背景：转录因子核因子-kappaB (NF-kappaB) 通过诱导各种细胞因子和生长因子参与炎症和免疫反应。本研究的目的是探讨免疫球蛋白 A (IgA) 肾病中 NF-kappaB 表达与组织损伤严重程度之间的相关性及其机制。方法：该研究纳入了28名患者的43份肾组织样本，其中IgA肾病28份，非IgA系膜增生性肾炎（非IgA肾病）5份，非增殖性肾炎（膜性肾病[MN] n = 5；微小病变肾病综合征[MCNS]；n = 5）10份。通过 Southwestern 组织化学和免疫组织化学检查组织切片中受 NF-κB 调节的单核细胞趋化蛋白-1 (MCP-1)、粒细胞巨噬细胞集落刺激因子 (GM-CSF) 和细胞间细胞粘附分子-1 (ICAM-1)。手术切除的患有腺癌的肾脏的正常部分作为对照。结果：在正常肾脏、MCNS和MN切片中，少数系膜细胞和肾小管上皮细胞检测到NF-κB表达。在IgA肾病和非IgA肾病样本中，NF-κB在系膜细胞、肾小球内皮细胞和上皮细胞、肾小管上皮细胞和浸润细胞中表达。肾小球和间质中的表达与组织损伤的进展相关。在 IgA 肾病样本中，肾小球和间质中的 MCP-1 和 GM-CSF 表达均增加，并且与组织损伤的进展相关。严重病变时肾小球 ICAM-1 表达较弱，而间质表达与组织损伤进展相关。结论：我们的结果表明 NF-kappaB 通过诱导转录调控基因参与 IgA 肾病组织损伤的进展。 (C) 2003 年，国家肾脏基金会 (National Kidney Foundation, Inc.)
Background: The transcription factor nuclear factor-kappaB (NF-kappaB) is involved in inflammatory and immune responses through induction of various cytokines and growth factors. The aim of this study is to examine the correlation between NF-kappaB expression and severity of tissue injury in immunoglobulin A (IgA) nephropathy and the mechanism of such correlation. Methods:The study included 43 renal tissue samples from 28 patients, including 28 samples of IgA nephropathy, 5 samples of non-IgA mesangial proliferative glomerulonephritis (non-IgA nephropathy), and 10 samples with nonproliferative glomerulonephritis (membranous nephropathy [MN] n = 5; minimal change nephrotic syndrome [MCNS]; n = 5). Tissue sections were examined by Southwestern histochemistry and immunohistochemistry for monocyte chemoattractant protein-1 (MCP-1), granulocyte-macrophage colony-stimulating factor (GM-CSF), and intercellular cell adhesion molecule-1 (ICAM-1), which are regulated by NF-kappaB. Normal portions of surgically resected kidney with adenocarcinoma served as controls. Results: In normal kidney, MCNS, and MN sections, NF-kappaB expression was detected in a few mesangial cells and tubular epithelial cells. In IgA nephropathy and non-IgA nephropathy samples, NF-kappaB was expressed in mesangial, glomerular endothelial and epithelial cells, tubular epithelial cells, and infiltrating cells. Expression in both glomeruli and interstitium correlated with progression of tissue injury. In IgA nephropathy samples, MCP-1 and GM-CSF expression was increased in both glomeruli and interstitium and correlated with progression of tissue injury. Glomerular ICAM-1 expression was weaker in severe lesions, whereas interstitial expression correlated with progression of tissue injury. Conclusion: Our results indicate that NF-kappaB is involved in the progression of tissue injury in IgA nephropathy through the induction of transcriptionally regulated genes. (C) 2003 by the National Kidney Foundation, Inc.