Renal ACE2 expression in human kidney disease
Renal ACE2 expression in human kidney disease
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DOI：
10.1002/path.1670
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发表时间：
2004-12-01
影响因子：
7.3
通讯作者：
Navis, GJ
中科院分区：
文献类型：
--
作者：
Lely, AT;Hamming, I;Navis, GJ
血管紧张素转换酶2(ACE2)是最近发现的一种血管紧张素转换酶(ACE)的同系物，被认为可以抵消ACE。血管紧张素转换酶2将血管紧张素I和血管紧张素11分别分解为失活的血管紧张素1-9，以及血管扩张剂和抗增殖的血管紧张素1-7。已知ACE2存在于人类肾脏中，但到目前为止还没有关于肾脏疾病的数据。本文对58例各种原发和继发性肾病患者(高血压肾病5例，IgA肾小球病变8例，微小病变型肾病7例，糖尿病肾病8例，局灶性肾小球硬化5例，血管炎7例，膜性肾小球病变18例)及17例移植肾和18例正常肾组织进行了肾活检。ACE2免疫组织化学染色半定量评分。在对照肾脏中，ACE2表达于肾小管和肾小球上皮细胞、血管平滑肌细胞和小叶间动脉内皮细胞。在所有原发和继发性肾脏疾病和肾移植中，ACE2在肾小球和肾小管周围毛细血管内皮细胞中均有新的表达。在各种肾脏疾病之间，或在急性和慢性排斥反应和对照移植之间没有差异。血管紧张素转换酶抑制剂处理不改变ACE2的表达。在原发和继发性肾脏疾病以及移植肾中，ACE2在肾小球和肾小管周围毛细血管内皮细胞中表达。进一步的研究应阐明ACE2从头表达在肾脏疾病中可能的保护机制。版权所有(C)2004年大不列颠和爱尔兰病理学会。作者：John Wiley Sons，Ltd.
Angiotensin-converting enzyme 2 (ACE2) is a recently discovered homologue of angiotensin- converting enzyme (ACE) that is thought to counterbalance ACE. ACE2 cleaves angiotensin I and angiotensin 11 into the inactive angiotensin 1-9, and the vasodilator and anti-proliferative angiotensin 1-7, respectively. ACE2 is known to be present in human kidney, but no data on renal disease are available to date. Renal biopsies from 58 patients with diverse primary and secondary renal diseases were studied (hypertensive nephropathy = 5, IgA glomerulopathy n = 8, minimal change nephropathy n = 7, diabetic nephropathy n = 8, focal glomerulosclerosis n = 5, vasculitis n = 7, and membranous glomerulopathy n = 18) in addition to 17 renal transplants and 18 samples from normal renal tissue. Immunohistochemical staining for ACE2 was scored semi-quantitatively. In control kidneys, ACE2 was present in tubular and glomerular epithelium and in vascular smooth muscle cells and the endothelium of interlobular arteries. In all primary and secondary renal diseases, and renal transplants, neo-expression of ACE2 was found in glomerular and peritubular capillary endothelium. There were no differences between the various renal disorders, or between acute and chronic rejection and control transplants. ACE inhibitor treatment did not alter ACE2 expression. In primary and secondary renal disease, and in transplanted kidneys, neo-expression of ACE2 occurs in glomerular and peritubular capillary endothelium. Further studies should elucidate the possible protective mechanisms involved in the de novo expression of ACE2 in renal disease. Copyright (C) 2004 Pathological Society of Great Britain and Ireland. Published by John Wiley Sons, Ltd.