ROLE OF LOX-1, A NOVEL OXIDIZED LOW-DENSITY LIPOPROTEIN RECEPTOR.IN THE PROGRESSION OF RENAL INJURY
新型氧化低密度脂蛋白受体LOX-1在肾损伤进展中的作用
基本信息
- 批准号:11671028
- 负责人:
- 金额:$ 2.24万
- 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:1999
- 资助国家:日本
- 起止时间:1999 至 2000
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
Oxidized low-density lipoprotein (OxLDL) has been implicated in atherosclerosis and glomerulosclerosis. LOX-1 is a recently identified OxLDL receptor abundantly expressed in vascular endothelial cells. We previously reported that LOX-1 expression was markedly enhanced in the vasculatures of hypertensive rats. The aim of the present study was to investigate LOX-1 expression in the kidneys of hypertensive rats. Dahl salt-sensitive (DS) and salt-resistant (DR) rats were fed a 0.3% or 8% NaCl diet. Some DS 8% rats were treated with manidipine or hydralazine. LOX-1 gene expression was markedly elevated in the kidneys and glomeruli of hypertensive DS 8% rats compared with those of normotensive DR and DS 0.3% rats. Prolonged salt loading further increased the renal LOX-1 expression in DS rats. The LOX-1 upregulation in DS 8% rats was accompanied by renal overexpression of transforming growth factor-β1 and type I collagen, impaired renal function, and histological glomerulosclerotic changes, all of which were ameliorated by anti-hypertensive treatment. LOX-1 was indeed expressed in the glomeruli in vivo and in cultured glomerular cells in vitro. On the other hand, LOX-1 expression was elevated in the aortas but not the kidneys of spontaneously hypertensive rats, which exhibited hypertension but minor glomerulosclerotic changes. In conclusion, the LOX-1 upregulation in the kidney of DS 8% rats was in parallel to glomerulosclerotic changes and renal dysfunction, suggesting a possible pathogenetic role for renal LOX-1 in the progression to hypertensive glomerulosclerosis.
氧化低密度脂蛋白(OxLDL)与动脉粥样硬化和肾小球硬化有关。LOX-1是最近发现的OxLDL受体,在血管内皮细胞中大量表达。我们之前报道了高血压大鼠血管中LOX-1的表达明显增强。本研究旨在探讨LOX-1在高血压大鼠肾脏中的表达。盐敏感大鼠(DS)和耐盐大鼠(DR)分别饲喂0.3%和8% NaCl日粮。一些DS 8%大鼠给予曼尼地平或肼嗪治疗。LOX-1基因在高血压DS大鼠肾脏和肾小球中的表达明显高于正常DR和DS大鼠0.3%。长期的盐负荷进一步增加了DS大鼠肾脏LOX-1的表达。DS大鼠LOX-1表达上调8%,伴有肾转化生长因子-β1和I型胶原的过度表达,肾功能受损,组织学肾小球硬化改变,抗高血压治疗均可改善。LOX-1确实在体内肾小球和体外培养肾小球细胞中表达。另一方面,自发性高血压大鼠主动脉中LOX-1表达升高,而肾脏中LOX-1表达不升高,表现为高血压,但肾小球硬化改变较小。综上所述,8% DS大鼠肾脏中LOX-1的上调与肾小球硬化改变和肾功能障碍平行,提示肾LOX-1可能在高血压性肾小球硬化的进展中起病理作用。
项目成果
期刊论文数量(6)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Nagase M et al: "Expression of LOX-1, an oxidized low-density lipoprotein receptor, in experimental hypertensive glomerulosclerosis"J Am Soc Nephrol. 11. 1826-1836 (2000)
Nagase M 等人:“实验性高血压肾小球硬化症中氧化低密度脂蛋白受体 LOX-1 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:
Nagase M et al: "Redox-sensitive regulation of LOX-1 gene expression in vascular endothelium"Biochem Biophys Res Commun. 281(3). 720-725 (2001)
Nagase M 等人:“血管内皮中 LOX-1 基因表达的氧化还原敏感调节”Biochem Biophys Res Commun。
- DOI:
- 发表时间:
- 期刊:
- 影响因子:0
- 作者:
- 通讯作者:
NAGASE METAL: "REDOX-SENSITIVE REGULATION OF LOX-1 GENE EXPRESSION IN VASCULAR ENDOTHELIUM"BIOCHEM BIOPHYS RES COMMUN. 283. 720-725 (2001)
NAGASE METAL:“血管内皮中 LOX-1 基因表达的氧化还原敏感调节”Biochem Biophys RES COMMUN。
- DOI:
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- 影响因子:0
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NAGASE Miki其他文献
NAGASE Miki的其他文献
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{{ truncateString('NAGASE Miki', 18)}}的其他基金
Elucidation of the pathogenesis and development of new diagnostic and therapeutic strategy of kidney disease based on mechanobiology
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- 批准号:
20K08616 - 财政年份:2020
- 资助金额:
$ 2.24万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Elucidation of mineralocorticoid receptor/ glucocorticoid receptor paradox and its application to kidney disease therapy
盐皮质激素受体/糖皮质激素受体悖论的阐明及其在肾脏疾病治疗中的应用
- 批准号:
24390214 - 财政年份:2012
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$ 2.24万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Strategy for overcoming chronic kidney disease, focusing on mineralocorticoid receptor
克服慢性肾脏病的策略,重点关注盐皮质激素受体
- 批准号:
21390261 - 财政年份:2009
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Glomerular podocyte injury in lifestyle-related disease : elucidation of its mechanism and establishment of novel therapeutic strategy to inhibit proteinuria
生活方式相关疾病中的肾小球足细胞损伤:阐明其机制并建立抑制蛋白尿的新治疗策略
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17590820 - 财政年份:2005
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$ 2.24万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
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