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I、II和III型转化生长因子-β受体在人类肾小球肾炎中的表达

Expression of types I, II, and III TGF-beta receptors in human glomerulonephritis.

作者信息

Yamamoto T, Watanabe T, Ikegaya N, Fujigaki Y, Matsui K, Masaoka H, Nagase M, Hishida A

机构信息

Division of Nephrology, Seirei Hamamatsu General Hospital, Shizuoka, Japan.

出版信息

J Am Soc Nephrol. 1998 Dec;9(12):2253-61. doi: 10.1681/ASN.V9122253.

DOI:10.1681/ASN.V9122253
PMID:9848779
Abstract

Protein and mRNA expression of transforming growth factor-beta (TGF-beta) receptor type I (TbetaRI), type II (TbetaRII), and type III (TbetaRIII) were studied in serial sections of kidney samples obtained from patients with glomerulonephritis. In minimal change disease, weak expression of TbetaRI and TbetaRII was observed mainly in glomerular endothelial cells, peritubular capillaries, and interstitial arteriolar endothelial cells, whereas TbetaRIII expression was found mainly in the interstitium. Expression of all three TGF-beta receptors (TbetaR) was increased remarkably in glomerular and Bowman's capsular cells comprising the tuft adhesions to Bowman's capsules in glomerulonephritis with increased matrix accumulation, including IgA nephropathy, lupus nephritis, focal and segmental glomerulosclerosis, myeloperoxidase-antineutrophil cytoplasmic antibody-associated crescentic glomerulonephritis, and membranoproliferative glomerulonephritis. Increased expression of the three TbetaR was also seen in glomerular epithelial cells in the vicinity of glomerulosclerotic lesions, in crescent cells, and in some tubules and infiltrative mononuclear cells found in the periglomerular and tubulointerstitial lesions with increased matrix deposition. In contrast, no remarkable TbetaRII expression was noted in mesangial proliferative lesions in IgA nephropathy, lupus nephritis, and membranoproliferative glomerulonephritis. These data suggest that distinctive modulation of TbetaR expression may be involved in the development of adhesive, sclerotic, and proliferative renal lesions in human glomerulonephritis.

摘要

在从肾小球肾炎患者获取的肾脏样本连续切片中,研究了转化生长因子-β(TGF-β)Ⅰ型受体(TβRI)、Ⅱ型受体(TβRII)和Ⅲ型受体(TβRIII)的蛋白质和信使核糖核酸(mRNA)表达。在微小病变病中,主要在肾小球内皮细胞、肾小管周围毛细血管和间质小动脉内皮细胞中观察到TβRI和TβRII的弱表达,而TβRIII表达主要见于间质。在包括IgA肾病、狼疮性肾炎、局灶节段性肾小球硬化、髓过氧化物酶-抗中性粒细胞胞质抗体相关性新月体性肾小球肾炎和膜增生性肾小球肾炎在内的伴有基质积聚增加的肾小球肾炎中,在与鲍曼囊形成簇状粘连的肾小球和鲍曼囊细胞中,所有三种TGF-β受体(TβR)的表达均显著增加。在肾小球硬化病变附近的肾小球上皮细胞、新月体细胞以及在肾小球周围和肾小管间质病变中发现的一些肾小管和浸润性单核细胞中,随着基质沉积增加,也可见三种TβR表达增加。相比之下,在IgA肾病、狼疮性肾炎和膜增生性肾小球肾炎的系膜增生性病变中,未观察到明显的TβRII表达。这些数据表明,TβR表达的独特调节可能参与了人类肾小球肾炎中粘连性、硬化性和增殖性肾病变的发生发展。

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