Glomerular NO synthase activity in mesangial cell immune injury.
Glomerular NO synthase activity in mesangial cell immune injury.
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肾小球NO合酶活性在系膜细胞免疫损伤中的作用。
DOI：
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发表时间：
1993
期刊：
影响因子：
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通讯作者：
Terence Cook
中科院分区：
文献类型：
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作者：
Cattell;E. Lianos;P. Largen;Terence Cook
离体肾小球合成亚硝酸盐（NO2-）提供了一氧化氮（NO）诱导肾小球肾炎（GN）的证据。在巨噬细胞相关性GN中，主要来源是浸润性巨噬细胞。由于NO合成的诱导现已显示在培养的系膜细胞，我们已经研究了是否在体内系膜增殖是NO2-的来源。静脉注射抗Thy1.1单克隆抗体ER 4诱导系膜增生性GN。在第4天（系膜溶解期）和第7天（系膜增殖）测定分离的肾小球的NO2合成和巨噬细胞浸润。在第4天，但不是在第7天，基础NO2-增加（8.3 +/- 1.8，对照组0.7 +/- 0.1 nmol/2，000个肾小球/48 h; p = 0.05），并且存在巨噬细胞浸润（60 +/- 15;对照组14个巨噬细胞/肾小球）。在这两个时间NO2-升高外源性IL-1或LPS，更显着的第4天比第7天。因此，系膜增生性病变不是基础NO2-的来源，巨噬细胞是最可能的来源。然而，NO2-可以诱导系膜增生肾小球由外源性刺激，结果类似于那些报道在培养的系膜细胞。正常大鼠的辐射实验表明，刺激的NO2-合成被抑制的巨噬细胞耗竭。因此，无论是在正常还是增生性肾小球系膜细胞的NO 2-生产的证据。
Ex vivo synthesis of nitrite (NO2-) by nephritic glomeruli provides evidence of induction of nitric oxide (NO) in glomerulonephritis (GN). In macrophage-associated GN, the major source is infiltrating macrophages. As induction of NO synthesis has now been shown in cultured mesangial cells, we have examined whether in vivo mesangial proliferation is a source of NO2-. Mesangial proliferative GN was induced by intravenous anti-Thy1.1 (monoclonal antibody ER4). Isolated glomeruli were assayed for NO2- synthesis and macrophage infiltration on day 4 (mesangiolytic phase) and on day 7 (mesangial proliferation). On day 4, but not on day 7, basal NO2- was increased (8.3 +/- 1.8, controls 0.7 +/- 0.1 nmol/2,000 glomeruli/48 h; p = 0.05) and there was macrophage infiltration (60 +/- 15; controls 14 macrophages/glomerulus). At both times NO2- was elevated by exogenous IL1 or LPS, more significantly on day 4 than on day 7. Thus, mesangial proliferative lesions are not a source of basal NO2-, and macrophages are the most likely source. However, NO2- can be induced in mesangial proliferative glomeruli by exogenous stimuli, findings similar to those reported in cultured mesangial cells. Irradiation experiments in normal rats show that stimulated NO2- synthesis is inhibited by macrophage depletion. Therefore in neither normal nor proliferative glomeruli is there evidence for mesangial cell production of NO2-.