Expression of endothelial and inducible nitric oxide synthase in human glomerulonephritis
Expression of endothelial and inducible nitric oxide synthase in human glomerulonephritis
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DOI：
10.1046/j.1523-1755.1998.00907.x
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发表时间：
1998-06-01
影响因子：
19.6
通讯作者：
Kohno, S
中科院分区：
文献类型：
--
作者：
Furusu, A;Miyazaki, M;Kohno, S
一氧化氮（NO）在肾脏中的存在与人类肾小球肾炎的发病机制有关。然而，在人类患病肾脏中，表达NO合酶（NOS）和参与NO局部产生的NOS亚型的肾小球细胞的确切类型尚未确定。我们检测了伊加肾病（IgAN，N = 10）、狼疮性肾炎（LN，N = 5）、膜性肾病（MN，N = 5）和微小病变型肾病综合征（MCNS，N = 5）患者肾组织中诱导型一氧化氮合酶（iNOS）、内皮型一氧化氮合酶（eNOS）和脑型一氧化氮合酶（bNOS）的表达。切片进行免疫染色，并检查各NOS的表达与该切片中肾小球损伤程度之间的相关性。手术切除的肾脏的正常部分作为对照。eNOS表达于对照组和病变组肾小球内皮细胞和皮质血管内皮细胞。iNOS定位于肾小球系膜细胞，肾小球上皮细胞和浸润细胞在病变的肾小球，而免疫组化iNOS几乎没有检测到在对照肾。此外，eNOS在各肾小球中的表达模式与iNOS相反。在IgAN和LN中，eNOS的表达与肾小球损伤程度呈负相关，iNOS的表达与肾小球损伤程度呈正相关，bNOS在正常和肾炎肾小球中均未检测到。我们的研究结果表明，在人类患病肾脏中存在NO通路，并表明，NO来源于eNOS和iNOS可能参与肾脏疾病的进展，并且NO来源于每个NOS可能以不同的方式在人类炎症肾小球中发挥重要作用。
The presence of nitric oxide (NO) in the kidney has been implicated in the pathogenesis of human glomerulonephritis. However, the exact type of glomerular cells that express NO synthase (NOS) and the NOS isoform involved in the local production of NO has not been identified in the human diseased kidney. We examined the expression of three isoforms of NOS, inducible NOS (iNOS), endothelial NOS (eNOS) and brain NOS (bNOS) in the renal tissue of patients with IgA nephropathy (IgAN, N = 10), lupus nephritis (LN, N = 5), membranous nephropathy (MN, N = 5) and minimal change nephrotic syndrome (MCNS, N = 5). Sections were immunostained and the correlation between the expression of each NOS and the degree of glomerular injury in that section was also examined. Normal portions of surgically resected kidneys served as controls. eNOS was present in glomerular endothelial cells and endothelium of cortical vessels in the control and diseased kidneys. iNOS was localized in mesangial cells, glomerular epithelial cells and infiltrating cells in the diseased glomeruli, whereas immunostaining for iNOS was hardly detected in control kidneys. In addition, the expression pattern of eNOS in each glomerulus was the reverse of that of iNOS. In IgAN and LN, the extent of staining for eNOS correlated negatively with the degree of glomerular injury, while the extent of staining for iNOS correlated positively with the degree of glomerular injury in the same tissues, bNOS was not detected in normal or nephritic glomeruli. Our results indicate the presence of a NO pathway in human diseased kidney, and suggest that NO derived from eNOS and iNOS may be involved in the progression of renal diseases and that NO derived from each NOS may play an important role in different way in human inflamed glomeruli.