PDGF-RECEPTOR LOCALIZES TO MESANGIAL, PARIETAL EPITHELIAL, AND INTERSTITIAL-CELLS IN HUMAN AND PRIMATE KIDNEYS
PDGF-RECEPTOR LOCALIZES TO MESANGIAL, PARIETAL EPITHELIAL, AND INTERSTITIAL-CELLS IN HUMAN AND PRIMATE KIDNEYS
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DOI：
10.1038/ki.1993.45
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发表时间：
1993-02-01
影响因子：
19.6
通讯作者：
BOWENPOPE, DF
中科院分区：
文献类型：
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作者：
ALPERS, CE;SEIFERT, RA;BOWENPOPE, DF
有证据表明，血小板衍生生长因子（PDGF）是人类疾病中肾动脉和肾系膜、实验性系膜增殖性肾小球肾炎中的系膜以及血管紧张素II介导的高血压啮齿动物模型中的间质增生性变化的介质。我们利用pdgf受体β亚基的单克隆抗体来定位该受体在人类和非人灵长类动物组织中的组成性表达。组织在2%或4%多聚甲醛的低温下固定，并在光镜和免疫电镜下采用免疫组织化学技术。在肾小球中，该分子在系膜细胞中广泛表达，并在顶壁上皮细胞的顶端和外侧表面频繁表达。这种分子也广泛表达于皮质和髓质小管周围间质细胞，但不表达于肾小球或小管周围毛细血管内皮或其他肾实质结构。能够在这些位点结合PDGF b链的受体的鉴定：(1)为人类疾病中PDGF介导的系膜增殖提供了基础；(2)为PDGF介导的间质细胞迁移和/或增殖和/或在小管间质损伤部位活化提供了基础；(3)提示肾小球壁上皮细胞可能对PDGF的刺激有反应。
There is evidence that platelet derived growth factor (PDGF) is a mediator of proliferative changes in renal arteries and mesangium in human disease, in the mesangium in experimental mesangial proliferative glomerulonephritis, and in the interstitium in a rodent model of angiotensin II mediated hypertension. We utilized a monoclonal antibody to the beta-subunit of the PDGF-receptor to localize constitutive expression of this receptor in human and nonhuman primate tissues. Tissues were fixed in cold 2 or 4% paraformaldehyde, and immunohistochemical techniques both at the light microscopic level and immunoelectron microscopy were employed. In the glomerulus, there is widespread expression of this molecule by mesangial cells, and there is frequent expression on the apical and lateral surface of parietal epithelial cells. There is also widespread expression of this molecule by cortical and medullary peritubular interstitial cells, but not by glomerular or peritubular capillary endothelium or other renal parenchymal structures. The identification of receptors capable of binding PDGF B-chain at each of these sites: (1) provides a basis for PDGF mediated mesangial proliferation in human disease; (2) provides a basis for PDGF mediated interstitial cell migration and/or proliferation and/or activation at sites of tubulointerstitial injury; and (3) suggests that glomerular parietal epithelial cells may be responsive to stimulation by PDGF.