Fibrogenic Growth Factors in Encapsulating Peritoneal Sclerosis

Fibrogenic Growth Factors in Encapsulating Peritoneal Sclerosis
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DOI:
10.1159/000228540
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发表时间:
2009-01-01
影响因子:
--
通讯作者:
Alscher, M. D.
Alscher, M. D.
中科院分区:
其他
文献类型:
--
作者:
Braun, N.;Reimold, F.;Alscher, M. D.

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背景资料:在动物模型中,纤维化生长激素的局部水平增加实质上有助于包裹腹膜硬化(EPS)的过程。研究方法:我们分析了来自具有正常肾功能(n = 10)、具有正常肾功能和炎症(n = 10)、PD无EPS(n = 10)和具有EPS(n = 9)的患者的探针。我们调查了纤维化的程度和血管和血管病变的数量。另外,我们还通过免疫组织化学方法检测了NF κ B、TGF β 1、TGF β 1受体、TGF β 2、TGF β 2受体、FGF-BP、CTGF和VEGF的表达。结果如下:在EPS中,我们发现VEGF的唯一上调(正常0,阑尾炎1.0 ± 1.2,PD 1.7 ± 1.8和EPS 5.7 ± 4.4; p < 0.0001),而在PD中,CTGF显著增加(正常6.0 ± 2.8,阑尾炎7.3 ± 2.5,PD 10.0 ± 1.8和EPS 7.3 ± 2.1; p = 0.0059)。TGF β系统和NF κ B的结果不一致,EPS中未证实增加。血管病变在EPS中明显更明显(正常0.4 ± 0.5,阑尾炎0.2 ± 0.3,PD 1.0 ± 0.7和EPS 1.6 ± 1.2; p < 0.0001)(正常30 +/- 16,阑尾炎82 +/- 48,PD 1,936 +/- 952和EPS 2,613 +/-1,209; p < 0.0001),而血管密度降低(正常125 +/- 114,阑尾炎817 +/- 347,PD 81 +/- 57和EPS 36 +/- 33; p < 0.0001)。结论:EPS的发生发展与腹膜组织VEGF的增加有关。与明显的纤维化相比,血管密度降低可能表明缺氧是一种诱导因素。版权所有(C)2009 S. Karger AG,巴塞尔
Background: Increased local levels of fibrogenic growth hormones contribute substantially to the process of encapsulating peritoneal sclerosis (EPS) in animal models. Methods: We analyzed probes from patients with normal kidney function (n = 10), with normal kidney function and inflammation (n = 10), on PD without (n = 10) and with EPS (n = 9). We investigated the degree of fibrosis and the number of vessels and vasculopathy. Additionally, we investigated the expression of NF kappa B, TGF beta 1, TGF beta 1 receptor, TGF beta 2, TGF beta 2 receptor, FGF-BP, CTGF and VEGF by immunohistochemistry. Results: In EPS, we found an exclusive upregulation of VEGF (normal 0, appendicitis 1.0 +/- 1.2, PD 1.7 +/- 1.8 and EPS 5.7 +/- 4.4; p < 0.0001), whereas in PD, CTGF was significantly increased (normal 6.0 +/- 2.8, appendicitis 7.3 +/- 2.5, PD 10.0 +/- 1.8 and EPS 7.3 +/- 2.1; p = 0.0059). The results for the TGF beta system and NF kappa B were not uniform, in EPS no increases were demonstrable. Vasculopathy was significantly more pronounced in EPS (normal 0.4 +/- 0.5, appendicitis 0.2 +/- 0.3, PD 1.0 +/- 0.7 and EPS 1.6 +/- 1.2; p < 0.0001) than in PD or inflammation (normal 30 +/- 16, appendicitis 82 +/- 48, PD 1,936 +/- 952 and EPS 2,613 +/- 1,209; p < 0.0001), whereas the density of vessels were decreased (normal 125 +/- 114, appendicitis 817 +/- 347, PD 81 +/- 57 and EPS 36 +/- 33; p < 0.0001). Conclusions: The process of EPS was associated with increased VEGF in the peritoneum. The reduced density of vessels compared with marked fibrosis could point to hypoxia as an inducer. Copyright (C) 2009 S. Karger AG, Basel