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本文引用的文献

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Contribution of the endothelium to the glomerular permselectivity barrier in health and disease.内皮细胞在健康和疾病状态下对肾小球滤过屏障的作用。
Nephron Physiol. 2007;106(2):p19-25. doi: 10.1159/000101796. Epub 2007 Jun 6.
2
Mutation in the key enzyme of sialic acid biosynthesis causes severe glomerular proteinuria and is rescued by N-acetylmannosamine.唾液酸生物合成关键酶的突变导致严重的肾小球蛋白尿,而N-乙酰甘露糖胺可挽救该症状。
J Clin Invest. 2007 Jun;117(6):1585-94. doi: 10.1172/JCI30954.
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Uncoupling of the VEGF-endothelial nitric oxide axis in diabetic nephropathy: an explanation for the paradoxical effects of VEGF in renal disease.糖尿病肾病中血管内皮生长因子-内皮型一氧化氮轴的解偶联:血管内皮生长因子在肾脏疾病中产生矛盾效应的一种解释。
Am J Physiol Renal Physiol. 2007 Jun;292(6):F1665-72. doi: 10.1152/ajprenal.00495.2006.
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Development of glomerular endothelial cells, podocytes and mesangial cells in the human fetus and infant.人胎儿和婴儿肾小球内皮细胞、足细胞和系膜细胞的发育
Tohoku J Exp Med. 2007 May;212(1):81-90. doi: 10.1620/tjem.212.81.
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Cell adhesion molecules in chemically-induced renal injury.化学诱导性肾损伤中的细胞黏附分子
Pharmacol Ther. 2007 Apr;114(1):74-93. doi: 10.1016/j.pharmthera.2007.01.001. Epub 2007 Jan 23.
6
Postinflammatory glomerular recanalization is established under the accommodation of transformed mesangial cells.炎症后肾小球再通是在转化的系膜细胞的调节下建立的。
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Involvement of mesangial cells expressing alpha-smooth muscle actin during restorative glomerular remodeling in Thy-1.1 nephritis.在Thy-1.1肾炎修复性肾小球重塑过程中表达α-平滑肌肌动蛋白的系膜细胞的参与情况。
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9
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Expression and localization of MT1-MMP and furin in the glomerular wall of short- and long-term diabetic rats.MT1-MMP和弗林蛋白酶在短期和长期糖尿病大鼠肾小球壁中的表达及定位
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短期和长期糖尿病中肾小球CD34的表达

Glomerular CD34 expression in short- and long-term diabetes.

作者信息

Acevedo Luz Marina, Londono Irene, Oubaha Malika, Ghitescu Lucian, Bendayan Moise

机构信息

Department of Pathology and Cell Biology, Université de Montréal, Montréal QC H3T 1J4, Canada.

出版信息

J Histochem Cytochem. 2008 Jun;56(6):605-14. doi: 10.1369/jhc.7A7354.2008. Epub 2008 Mar 3.

DOI:10.1369/jhc.7A7354.2008
PMID:18319274
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2386768/
Abstract

Aging and diabetes are associated with exacerbated expression of adhesion molecules. Given their importance in endothelial dysfunction and their possible involvement in the alteration of glomerular permeability occurring in diabetes, we have evaluated expression of the sialomucin-type adhesion molecule CD34 in renal glomerular cells of normal and diabetic animals at two different ages by colloidal gold immunocytochemistry and immunoblotting. CD34 labeling was mostly assigned to the plasma membranes of glomerular endothelium and mesangial processes. Podocyte membranes were also labeled, but to a lesser degree. Short- and long-term diabetes triggers a substantial increase in immunogold labeling for CD34 in renal tissues compared with young normoglycemic animals. However, the level of labeling in old diabetic and healthy control rats is similar, suggesting that the effect of diabetes and aging on CD34 expression is similar but not synergistic. Western blotting of isolated glomerular fractions corroborated immunocytochemical results. Increased expression of CD34 may reflect its involvement in the pathogenesis of glomerular alterations related to age and diabetes. Alterations present in early diabetes, resembling those occurring with age, strengthen the concept that diabetes is an accelerated form of aging.

摘要

衰老和糖尿病与黏附分子表达加剧有关。鉴于它们在内皮功能障碍中的重要性以及可能参与糖尿病时肾小球通透性的改变,我们通过胶体金免疫细胞化学和免疫印迹法评估了两种不同年龄的正常和糖尿病动物肾小球细胞中唾液黏蛋白型黏附分子CD34的表达。CD34标记主要定位于肾小球内皮和系膜突起的质膜。足细胞膜也有标记,但程度较轻。与年轻血糖正常的动物相比,短期和长期糖尿病会导致肾组织中CD34免疫金标记显著增加。然而,老年糖尿病大鼠和健康对照大鼠的标记水平相似,这表明糖尿病和衰老对CD34表达的影响相似,但并非协同作用。对分离的肾小球部分进行的蛋白质印迹分析证实了免疫细胞化学结果。CD34表达增加可能反映其参与了与年龄和糖尿病相关的肾小球改变的发病机制。早期糖尿病中出现的改变类似于衰老时发生的改变,强化了糖尿病是衰老加速形式的概念。