Molecular analysis and clinical application of LR11 in SMCs.
SMCs中LR11的分子分析及临床应用。
基本信息
- 批准号:17590917
- 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:2005
- 资助国家:日本
- 起止时间:2005 至 2006
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
The aim of study is to clarify the molecular mechanism of LR11, a gene specifically expressed in intimal SMCs, in the development of atherosclerosis.1. Establishment and characterization of LR11 knockout mice.The exon 1 of LR11 gene was replaced by NEO gene. The birth and growth properties of LR11-/- mice did not show any obvious difference from those of LR11+/+ mice. The intimal thickness after cuff injury in LR11-/- mice was significantly reduced compared with that in LR11+/+ mice. The cultured LR11-/- SMCs showed a significant decrease in migration activity under PDGF-BB stimulation compared with the LR11+/+ SMCs,2. The functional analyses of secreted soluble form of LR11A secreted soluble form of LR11 was established by the deletion of membrane-spanning and intracellular regions. The soluble form showed the inducing activity for migration, attachment and lipd incorporation of cultured macrophages, in addition to the migration activity of SMCs.3. Regulation of LR11 gene in SMCs.The LR11 gene transcription was significantly increased by PDGF-BB, and the increased transcription was inhibited by the treatment of pitavastatin. The LR11-overexpressing SMCs showed the decreased response to pitavastatin for migration activity.These results show that the aim of study could be almost completed in the study years.
本研究的目的是阐明LR 11基因在动脉粥样硬化发生发展中的分子机制. LR 11基因敲除小鼠的建立与鉴定LR 11基因第1外显子被NEO基因取代。LR 11-/-小鼠的出生和生长特性与LR 11 +/+小鼠无明显差异。与LR 11 +/+小鼠相比,LR 11-/-小鼠的袖套损伤后内膜厚度显著降低。与LR 11 +/+ SMCs相比,LR 11-/- SMCs在PDGF-BB刺激下的迁移活性显著降低。通过缺失跨膜区和胞内区,建立了分泌型可溶性LR 11 A的功能分析。可溶性形式除具有SMCs的迁移活性外,还具有诱导巨噬细胞迁移、粘附和脂质体掺入的活性.平滑肌细胞中LR 11基因的调控:PDGF-BB可显著增加LR 11基因的转录,匹伐他汀可抑制这种增加。LR 11过表达的SMC对匹伐他汀的迁移活性反应性降低,表明本研究的目的在本研究年内基本可以完成。
项目成果
期刊论文数量(11)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
A Selected Soluble Form of LR11, Specifically Expressed in Intimal Smooth Muscle Cells Accelerates Formation of Lipid - Laden Macrophages.
精选的 LR11 可溶形式,在内膜平滑肌细胞中特异性表达,可加速富含脂质的巨噬细胞的形成。
- DOI:
- 发表时间:2007
- 期刊:
- 影响因子:0
- 作者:Ohwaki K;Bujo H;Yamazaki H;Schneider WJ;Saito Y.
- 通讯作者:Saito Y.
A potent activator of PPARalpha and gamma reduces the vascular cell recruitment and inhibits the intimal thickning in hypercholesterolemic rabbits.
PPARα 和 γ 的有效激活剂可减少高胆固醇血症兔的血管细胞募集并抑制内膜增厚。
- DOI:
- 发表时间:2005
- 期刊:
- 影响因子:0
- 作者:Seki N;Bujo H;Jiang M;Shibasaki M;Takahashi K;Hashimoto N;Saito Y.
- 通讯作者:Saito Y.
A secreted soluble form of LR11, specifically expressed in intimal smooth muscle cells, accelerates formation of lipid-laden macrophages
- DOI:10.1161/atvbaha.106.137091
- 发表时间:2007-05-01
- 期刊:
- 影响因子:8.7
- 作者:Ohwaki, Kenji;Bujo, Hideaki;Saito, Yasushi
- 通讯作者:Saito, Yasushi
Modulation of smooth muscle cell migration by members of the low-density lipoprotein receptor family.
- DOI:10.1161/01.atv.0000219692.78477.17
- 发表时间:2006-06
- 期刊:
- 影响因子:0
- 作者:H. Bujo;Y. Saito
- 通讯作者:H. Bujo;Y. Saito
Pitavastatin attenuates the PDGF-induced LR11/uPA receptor-mediated migration of smooth muscle cells
- DOI:10.1016/j.bbrc.2006.07.204
- 发表时间:2006-10-06
- 期刊:
- 影响因子:3.1
- 作者:Jiang, Meizi;Bujo, Hideaki;Saito, Yasushi
- 通讯作者:Saito, Yasushi
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BUJO Hideaki其他文献
BUJO Hideaki的其他文献
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{{ truncateString('BUJO Hideaki', 18)}}的其他基金
Examinational significance and production mechanism of a circulating soluble receptor for the diagnosis of activated adipocytes to prevent diabetes
循环可溶性受体对诊断激活脂肪细胞预防糖尿病的检测意义和产生机制
- 批准号:
16H05231 - 财政年份:2016
- 资助金额:
$ 2.24万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Identification of the pathologically-transited immature cells diagnosed by soluble LR11
可溶性LR11诊断的病理转移未成熟细胞的鉴定
- 批准号:
15K15198 - 财政年份:2015
- 资助金额:
$ 2.24万 - 项目类别:
Grant-in-Aid for Challenging Exploratory Research
Molecular clarification of trans-differentiation to brown adipocytes through the action of soluble receptor LR11
通过可溶性受体 LR11 的作用对棕色脂肪细胞转分化的分子澄清
- 批准号:
24390231 - 财政年份:2012
- 资助金额:
$ 2.24万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Regulation of cellular cytoskeleton by the soluble LDL receptor family with the application for novel anti-atherosclerosis therapy
可溶性低密度脂蛋白受体家族对细胞骨架的调节及其在新型抗动脉粥样硬化治疗中的应用
- 批准号:
21390277 - 财政年份:2009
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$ 2.24万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Amelioration of pathological phenotypes of vascular smooth muscle cells by the sLR11 regulation
sLR11调节改善血管平滑肌细胞的病理表型
- 批准号:
19591036 - 财政年份:2007
- 资助金额:
$ 2.24万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Functional analysis of LR11 in vascular smooth muscle cells
LR11在血管平滑肌细胞中的功能分析
- 批准号:
12835002 - 财政年份:2000
- 资助金额:
$ 2.24万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Functional analysis of the brain-specific LDL receptor family memners
脑特异性 LDL 受体家族成员的功能分析
- 批准号:
09671027 - 财政年份:1997
- 资助金额:
$ 2.24万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
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