Department of Histology and Embryology, Cerrahpasa Faculty of Medicine, Istanbul University, Turkey.
J Biomed Sci. 2012 Feb 16;19(1):24. doi: 10.1186/1423-0127-19-24.
In experimentally induced puromycine aminonucleoside nephrosis (PAN) animal models, nephrotic syndrome with minimal change disease and focal and segmental sclerosis-like nephritis similar to that in human is demonstrated; however, the real mechanism of PAN is not yet elucidated. Platelet derived endothelial cell growth factor (PD-ECGF), an endothelial mitogen protein, is believed to take part in microvessel formation and in stimulation of angiogenesis and its expression has not been totally demonstrated in PAN rats yet. In this study, we aimed to examine PD-ECGF expression in acute and chronic PAN induced in rats and find out the association between its expression and the stages of angiogenesis in kidney.
For the experiment, twenty-four Male Wistar Albino rats were used and divided into four groups; control group (n = 6), pre-proteinuria group (n = 6), acute group (n = 6) and chronic group (n = 6). We compared statistically all data by One-way ANOVA Test followed by Dunn Multiple Comparison Test.
Proteinurea levels in control and pre-proteinuria groups were not statistically different; however, it was remarkably higher in the acute nephrosis group and significantly greater in the chronic nephrosis group than control group (p < 0.0025). In pre-proteinuria group, the serum albumin and creatinine clearances also did not significantly differ from the control group. On the other hand, in the acute and chronic nephrosis groups, serum albumin and creatinine clearances progressively decreased (p < 0.05). In our immunohistochemical studies, we showed elevated PD-ECGF expression in glomeruli of acute and chronic PAN rats. Microscopic and ultrastructural appearances of the glomeruli of acute and chronic PAN showed various sequential steps of angiogenesis, macrophages and immature capillaries with primitive lumens and apoptotic endothelial cells in the increased mesangial matrix.
It is reported that acute and chronic PAN progressively increase PD-ECGF expression and following induction of angiogenesis in the affected glomeruli.
在实验诱导的嘌呤霉素氨基核苷肾病 (PAN) 动物模型中，表现出类似于人类的肾病综合征伴微小病变和局灶节段性硬化样肾炎；然而，PAN 的真正机制尚未阐明。血小板衍生的内皮细胞生长因子 (PD-ECGF)，一种内皮细胞有丝分裂原蛋白，被认为参与微血管形成和血管生成的刺激，其在 PAN 大鼠中的表达尚未完全证实。在这项研究中，我们旨在检查 PD-ECGF 在大鼠诱导的急性和慢性 PAN 中的表达，并找出其表达与肾脏血管生成阶段之间的关系。
在实验中，使用 24 只雄性 Wistar 白化大鼠，并将其分为四组；对照组 (n = 6)、蛋白尿前组 (n = 6)、急性组 (n = 6) 和慢性组 (n = 6)。我们通过单因素方差分析检验对所有数据进行了统计学比较，然后进行了 Dunn 多重比较检验。
对照组和蛋白尿前组的蛋白尿水平无统计学差异；然而，在急性肾病组中显著升高，在慢性肾病组中显著高于对照组 (p < 0.0025)。在蛋白尿前组中，血清白蛋白和肌酐清除率也与对照组无显著差异。另一方面，在急性和慢性肾病组中，血清白蛋白和肌酐清除率逐渐降低 (p < 0.05)。在我们的免疫组织化学研究中，我们显示了急性和慢性 PAN 大鼠肾小球中 PD-ECGF 表达的升高。急性和慢性 PAN 肾小球的微观和超微结构表现为血管生成的各种连续步骤，在增加的系膜基质中可见巨噬细胞和不成熟毛细血管与原始管腔和凋亡的内皮细胞。
据报道，急性和慢性 PAN 逐渐增加 PD-ECGF 表达，并在受影响的肾小球中诱导血管生成。
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