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血小板介导大鼠抗系膜细胞抗体诱导的免疫复合物性肾炎中的肾小球细胞增殖。

Platelets mediate glomerular cell proliferation in immune complex nephritis induced by anti-mesangial cell antibodies in the rat.

作者信息

Johnson R J, Garcia R L, Pritzl P, Alpers C E

机构信息

Department of Medicine, University of Washington, Seattle 98195.

出版信息

Am J Pathol. 1990 Feb;136(2):369-74.

PMID:1968315
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1877401/
Abstract

We investigated whether platelets, which are rich in growth factors, could mediate glomerular cell proliferation in immune complex glomerulonephritis (GN) in the rat induced with an antibody directed against the Thy-1 antigen present on mesangial cells. Rats were depleted of platelets (mean platelet count less than 20,000/mm3) with goat anti-rat platelet IgG before induction of GN and platelet depletion was maintained for 48 hours. At 72 hours sections were immunostained for cyclin, an S-phase-related nuclear antigen, to identify proliferating cells, and for the common leukocyte antigen (CD45) to identify infiltrating leukocytes. Platelet depleted rats had fewer proliferating resident glomerular cells (CD45-, cyclin+) compared to controls (0.8 +/- 0.5 vs. 2.8 +/- 1.4 cells/glom cross section, P less than 0.01) and better renal function (creatinine 1.07 +/- 0.12 vs. 1.27 +/- 0.15 mg/dl, P less than 0.05). These effects were not due to changes in circulating or glomerular leukocyte counts, complement, or glomerular antibody binding. These studies provide the first direct evidence that platelets mediate glomerular (probably mesangial cell) proliferation in antibody-mediated GN.

摘要

我们研究了富含生长因子的血小板是否能介导大鼠免疫复合物性肾小球肾炎(GN)中的肾小球细胞增殖。该肾炎是通过针对系膜细胞上存在的Thy-1抗原的抗体诱导产生的。在诱导GN之前,用山羊抗大鼠血小板IgG使大鼠血小板减少(平均血小板计数小于20,000/mm³),并维持血小板减少状态48小时。在72小时时,对切片进行免疫染色,检测细胞周期蛋白(一种与S期相关的核抗原)以识别增殖细胞,检测共同白细胞抗原(CD45)以识别浸润的白细胞。与对照组相比,血小板减少的大鼠增殖的肾小球固有细胞(CD45阴性、细胞周期蛋白阳性)较少(0.8±0.5对2.8±1.4个细胞/肾小球横截面,P<0.01),且肾功能更好(肌酐1.07±0.12对1.27±0.15mg/dl,P<0.05)。这些效应并非由于循环或肾小球白细胞计数、补体或肾小球抗体结合的变化所致。这些研究提供了首个直接证据,表明血小板在抗体介导的GN中介导肾小球(可能是系膜细胞)增殖。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b66/1877401/0076849a1db5/amjpathol00110-0120-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b66/1877401/0800c64215c4/amjpathol00110-0120-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b66/1877401/0076849a1db5/amjpathol00110-0120-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b66/1877401/0800c64215c4/amjpathol00110-0120-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8b66/1877401/0076849a1db5/amjpathol00110-0120-b.jpg

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本文引用的文献

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Cellular aspects of rabbit Masugi nephritis. II. Progressive glomerular injuries with crescent formation.兔肾毒血清性肾炎的细胞方面。II. 伴有新月体形成的进行性肾小球损伤。
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VEGF(165) mediates glomerular endothelial repair.血管内皮生长因子(165)介导肾小球内皮修复。
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