Role of adhesion morecule between glomerular epithelial cells and basement membrane, and cytoskeleton in proteinuria
肾小球上皮细胞与基底膜间的粘附细胞及细胞骨架在蛋白尿中的作用
基本信息
- 批准号:10671008
- 负责人:
- 金额:$ 1.92万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for Scientific Research (C)
- 财政年份:1998
- 资助国家:日本
- 起止时间:1998 至 1999
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
Proteiuria is a hallmark of glomerulonephritis, and induces progressive renal insufficiency. It is believed that the mechanism of urinary protein excretion is the disorder of permeability of glomerular capillary wall, but its precise mechanism is still unclear. Recently hyperpermeability of glomerular capillary wall is due to the disorder of glomerular epithelial cell and glomerular basement membrane. It is widely known that the epithelial cells detach from basement membrane in proteiuric state. This may be due to somehow derangement of attachment between epithelial cells and basement membrane. Recently it is reported that integrin family plays an important role for keeping attachment of epithelial cell and basement membrane. In this report we describe the amount and status of integrin expression in glomeruli.PAN nephrosis and passive Heymann nephrosis were induced in rats and immunofluorescence was carried out on the kidney sections from PAN nephrosis at day 3 and 7, from Heymann nephrosis at day 4 and 7. The sections were observed by confocal laser microscopy and data were analyzed computerized image analyzer. The amount of integrin expression has increased at day 3 of PAN nephrosis, but the linear like expression diminished which is observed on normal rat kidney. At day 7 the linear like pattern recovered. On the section of Heymann nephrosis at day 4, the amount of its expression decreased and day 7 the glanular pattern was observed in the epithelial cells. These results strongly indicated the pattern of integrin expression at glomerular capillary walls is more important than its amount.
蛋白尿是肾小球肾炎的标志,并引起进行性肾功能不全。目前认为,尿蛋白排泄的机制是肾小球毛细血管壁通透性的紊乱,但其确切机制尚不清楚。近年来肾小球毛细血管壁通透性增高是由于肾小球上皮细胞和肾小球基底膜结构紊乱所致。众所周知,上皮细胞在蛋白尿状态下与基底膜分离。这可能是由于上皮细胞与基底膜之间的附着紊乱所致。近年来研究发现,整合素家族在维持上皮细胞与基底膜的粘附中起重要作用。在这份报告中,我们描述的数量和状态的整合素的表达在肾小球。PAN肾病和被动Heymann肾病诱导大鼠和免疫荧光进行了肾切片从PAN肾病在第3和7天,从Heymann肾病在第4和7天。用激光共聚焦显微镜观察切片,计算机图像分析仪分析数据。在PAN肾病的第3天,整合素的表达量增加,但在正常大鼠肾脏中观察到的线性样表达减少。在第7天,线性样图案恢复。在Heymann肾病第4天的切片上,其表达量减少,第7天在上皮细胞中观察到腺状图案。这些结果有力地表明整合素在肾小球毛细血管壁的表达模式比其数量更重要。
项目成果
期刊论文数量(23)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Nakamura K: "Dipyridamole and dilazep suppress oxygen radicals in puromycin aminonucleoside nephrosis rats"Euro. J. Clin. Invest.. 28. 877-883 (1998)
Nakamura K:“双嘧达莫和地拉西普可抑制嘌呤霉素氨基核苷肾病大鼠中的氧自由基”Euro。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Yamamoto T.: "Expression of Types I,II and III TGF-beta receptors in human glonerulonephritis"J.Am.Soc.Nephrol. 9. 2253-2261 (1998)
Yamamoto T.:“人肾小球肾炎中 I、II 和 III 型 TGF-β 受体的表达”J.Am.Soc.Nephrol。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Kojima K: "Protection of α3-integrin-mediated podocyte sharpe by SOD in the puromycin aminonucleoside nephros rat"Am. J. kidney Dis. (in press).
Kojima K:“嘌呤霉素氨基核苷肾大鼠中 SOD 对 α3-整合素介导的足细胞锐利的保护”Am.J. 肾病。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Fujigaki Y: "Altered anionic GBM components in monocloral antibody against slit diaphragm-injected proteinuric rats." Kidney Int.54・5. 1491-1500 (1998)
Fujigaki Y:“针对裂隙隔膜注射蛋白尿大鼠的单克隆抗体中阴离子 GBM 成分的改变。”Kidney Int.54·5(1998)。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
Yamamoto T.: "MPO-ANCA-positive crescentic necretizing glomerulonephritis and tubuls interstitial Nephritis with renal cosinophilic infiltration and peripheral blood eosinophilir" Am.J.Kidney Dis. 31・6. 1032-1037 (1998)
Yamamoto T.:“MPO-ANCA 阳性新月体坏死性肾小球肾炎和肾小管间质性肾炎伴肾嗜酸性粒细胞浸润和外周血嗜酸性粒细胞”Am.J.Kidney Dis. 1032-1037。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
{{
item.title }}
{{ item.translation_title }}
- DOI:
{{ item.doi }} - 发表时间:
{{ item.publish_year }} - 期刊:
- 影响因子:{{ item.factor }}
- 作者:
{{ item.authors }} - 通讯作者:
{{ item.author }}
数据更新时间:{{ journalArticles.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ monograph.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ sciAawards.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ conferencePapers.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ patent.updateTime }}
NAGASE Mitsumasa其他文献
NAGASE Mitsumasa的其他文献
{{
item.title }}
{{ item.translation_title }}
- DOI:
{{ item.doi }} - 发表时间:
{{ item.publish_year }} - 期刊:
- 影响因子:{{ item.factor }}
- 作者:
{{ item.authors }} - 通讯作者:
{{ item.author }}
{{ truncateString('NAGASE Mitsumasa', 18)}}的其他基金
Regulation of Free Radical Production in Experimental Renal Disease
实验性肾病中自由基产生的调节
- 批准号:
06671153 - 财政年份:1994
- 资助金额:
$ 1.92万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Effect of Glomerular Capillary Wall Alteration on the Distribution of Immune Complex
肾小球毛细血管壁改变对免疫复合物分布的影响
- 批准号:
62570283 - 财政年份:1987
- 资助金额:
$ 1.92万 - 项目类别:
Grant-in-Aid for General Scientific Research (C)
相似国自然基金
Regulator of Lupus Nephritis 在狼疮性肾炎中的作用及其机制的研究
- 批准号:81970599
- 批准年份:2019
- 资助金额:55.0 万元
- 项目类别:面上项目
相似海外基金
Treatment of lupus nephritis with nanoparticles that selectively target kidney glomeruli
用选择性靶向肾小球的纳米颗粒治疗狼疮性肾炎
- 批准号:
10679184 - 财政年份:2023
- 资助金额:
$ 1.92万 - 项目类别:
Pathogenic role of innate immune cells in lupus nephritis
先天免疫细胞在狼疮性肾炎中的致病作用
- 批准号:
10385854 - 财政年份:2019
- 资助金额:
$ 1.92万 - 项目类别:
Pathogenic role of innate immune cells in lupus nephritis
先天免疫细胞在狼疮性肾炎中的致病作用
- 批准号:
10132979 - 财政年份:2019
- 资助金额:
$ 1.92万 - 项目类别:
Pathogenic role of innate immune cells in lupus nephritis
先天免疫细胞在狼疮性肾炎中的致病作用
- 批准号:
9925183 - 财政年份:2019
- 资助金额:
$ 1.92万 - 项目类别:
Pathogenic role of innate immune cells in lupus nephritis
先天免疫细胞在狼疮性肾炎中的致病作用
- 批准号:
10601014 - 财政年份:2019
- 资助金额:
$ 1.92万 - 项目类别:
Defining glomerulus-homing peptides for targeted drug delivery in lupus nephritis
定义用于狼疮性肾炎靶向药物递送的肾小球归巢肽
- 批准号:
8787075 - 财政年份:2013
- 资助金额:
$ 1.92万 - 项目类别:
NEPHROTOXIC NEPHRITIS IN CCR5 AND CXCR3 KNOCKOUT MICE
CCR5 和 CXCR3 敲除小鼠中的肾毒性肾炎
- 批准号:
6667079 - 财政年份:2001
- 资助金额:
$ 1.92万 - 项目类别:
NEPHROTOXIC NEPHRITIS IN CCR5 AND CXCR3 KNOCKOUT MICE
CCR5 和 CXCR3 敲除小鼠中的肾毒性肾炎
- 批准号:
6208122 - 财政年份:2000
- 资助金额:
$ 1.92万 - 项目类别:














{{item.name}}会员




