suPAR和WT1改变足细胞的粘附,并与IV类狼疮性肾炎的蛋白尿有关。

IF 4.7 Q2 IMMUNOLOGY Journal of Translational Autoimmunity Pub Date : 2023-10-13 DOI:10.1016/j.jtauto.2023.100216
Juan-José Bollain-y-Goytia , Felipe-de-Jesús Torres-Del-muro , Sara-Paola Hernández-Martínez , Esperanza Avalos-Díaz , Rafael Herrera-Esparza
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引用次数: 0

摘要

引言:高达60%的系统性红斑狼疮(SLE)患者患有狼疮性肾炎(LN),肾损伤进展与蛋白尿有关,部分原因是肾小球基底膜(GBM)的完整性和足细胞损伤。可溶性尿激酶纤溶酶原激活物受体(suPAR)和肾母细胞瘤1(WT1)与足细胞消失有关,因此与蛋白尿有关,这引发了人们对其在LN中的致病作用的质疑。目的:确定suPAR水平和WT1表达是否影响LN IV级足细胞锚定不稳定。材料和方法:这是一项病例和对照的横断面研究。我们研究了无肾脏受累的SLE患者(n=12)、蛋白尿≤0.5 g/24 h的SLE和LN IV级患者(n=2)、蛋白蛋白尿≥0.5 g/24小时的LN IV级病例(n=12。CR由没有SLE或肾脏受累的尸体样本整合,CS由健康参与者整合。免疫组织化学(IHC)检测WT1、尿激酶型纤溶酶原激活物受体(uPAR)、ac-α-微管蛋白、波形蛋白和β3-整合素的表达和细胞定位。采用酶联免疫吸附法(ELISA)测定血清中suPAR的浓度。结果:LN患者的锚定蛋白如足细胞β3-整合素的激活增加,α-乙酰微管蛋白和uPAR的乙酰化增加,而波形蛋白的激活减少;有趣的是,WT1的细胞定位是细胞质的,每个肾小球的足细胞数量减少。LN患者的suPAR浓度升高。结论:由β3-整合素激活和微管蛋白乙酰化调节的足细胞锚定的不稳定,与WT1细胞质表达的降低和suPAR水平的升高有关,可能与LN IV级患者的肾损伤有关。
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suPAR and WT1 modify the adhesion of podocytes and are related to proteinuria in class IV lupus nephritis

Introduction

Lupus nephritis (LN) affects up to 60 % of the patients with Systemic Lupus Erythematosus (SLE) and renal damage progression is associated with proteinuria, caused in part by the integrity of the glomerular basement membrane (GBM) and by podocyte injury. The soluble urokinase plasminogen activator receptor (suPAR) and Wilms Tumor 1 (WT1) have been related to podocyte effacement and consequently with proteinuria which raises questions about its pathogenic role in LN.

Objective

Define whether suPAR levels and WT1 expression influence in podocyte anchorage destabilization in LN class IV.

Materials and methods

This is a cross-sectional study of cases and controls. We studied patients with SLE without renal involvement (n = 12), SLE and LN class IV with proteinuria ≤0.5 g/24 h (n = 12), LN class IV with proteinuria ≥0.5 g/24 h (n = 12) and compared them with renal tissue control (CR) (n = 12) and control sera (CS) (n = 12). The CR was integrated by cadaveric samples without SLE or renal involvement and the CS was integrated by healthy participants. The expression and cellular localization of WT1, urokinase-type plasminogen activator receptor (uPAR), ac-α-tubulin, vimentin, and β3-integrin was assessed by immunohistochemistry (IHC). The concentration of suPAR in serum was analyzed by enzyme-linked immunosorbent assay (ELISA).

Results

In patients with LN, the activation of anchoring proteins was increased, such as podocyte β3-integrin, as well as the acetylation of alpha-acetyl-tubulin and uPAR, in contrast to the decrease in vimentin; interestingly, the cellular localization of WT1 was cytoplasmic and the number of podocytes per glomerulus decreased. The concentrations of suPAR was increased in patients with LN.

Conclusion

The destabilization of podocyte anchorage modulated by β3-integrin activation, and tubulin acetylation, associated with decreased WT1 cytoplasmic expression, and increased suPAR levels could be involved in kidney damage in patients with LN class IV.

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来源期刊
Journal of Translational Autoimmunity
Journal of Translational Autoimmunity Medicine-Immunology and Allergy
CiteScore
7.80
自引率
2.60%
发文量
33
审稿时长
55 days
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