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Regulation of Arterial Smooth Muscle Cell Proliferation in the Intima in Patients with Occlusion of Circle of Willis (Moyamoya Disease).

威利斯环闭塞（烟雾病）患者内膜动脉平滑肌细胞增殖的调节。

基本信息

批准号：
02807326
负责人：
AOGAKI Masaru
金额：
$ 0.32万
依托单位：
Tokyo Medical & Dental University, School of Medicine
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1990
资助国家：
日本
起止时间：
1990 至 1991
项目状态：
已结题

项目摘要

We have established each of five strains of smooth muscle cells derived fi-om arteries of patients with moyamoya and the control. The arterial specimens were obtained from branches of superficial temporal arteries. Biological natures and the response to growth factors of these cells were examined and compared with those of the controls. Both of the strains fi-om moyamoya and the controls have a limited life span in vitro. No difference was observed in the longevity of fmal population doubling levels(PDL). SMC from patients with moyamoya disease proliferated less in a medium supplemented with 15% serum than did control SMC and responded poorly to the addition of PDGF to 5% serum. PDGF alone did not stimulate SMC in a quiescent state to initiate DNA synthesis in moyainoya disease, without serum factors other than bovine serum albumin, though it significantly stimulated the controls. Simultaneous additions of EGF, IGF-1, and PDGF stimulated initiation of DNA synthesis in cells from moyamoya disease, but not as much as PDGF alone did in the controls. Receptor assay using ^<125>-I PDGF-BB demonstrated lower receptor number per cells in SMC of moyamoya than in controls. Apparent dissociation constant was not different between moyamoya and the controls. Although processing of ^<125>-1 PDGF in each receptor was not different between moyamoya and the controls, the PDGF receptor of moyamoya SMC was highly downregulated when exposed to low concentrations of PDGF at 37ﾟC, prior to binding to ^<125>-I PDGF. These results indicate altered regulations in cellular responses to PDGF, and may indicate a delayed repair of the injured vascular wall, resulting in a slower, but somewhat longer-terin rate of intimal proliferation in arteries of patients with moyamoya disease.

我们分别从烟雾患者和对照组的动脉建立了五种来源的平滑肌细胞。动脉标本取自颞浅动脉的分支。检测这些细胞的生物学特性和对生长因子的反应，并与对照组进行比较。FI-Moyamoya菌株和对照在体外都有有限的寿命。在正常种群倍增水平(PDL)的寿命方面没有差异。烟雾病患者的SMC在含15%血清的培养液中的增殖低于对照组，且对添加5%血清的PDGF反应较差。在没有血清因素的情况下，PDGF单独刺激静止状态的SMC启动烟雾病的DNA合成，尽管它显著地刺激了对照组。同时添加EGF、IGF-1和PDGF可刺激烟雾病患者细胞DNA合成的启动，但不像对照组中单独使用PDGF那么大。用~(125)&gt；-I PDGF-BB进行受体检测，发现烟雾病组SMC的每细胞受体数低于对照组。Moyamoya组和对照组的表观解离常数无明显差异。尽管烟雾病患者各受体上PDGF的表达与对照组无明显差异，但在37ﾟC低浓度的PDGF作用下，烟雾病SMC的PDGF受体在与PDGF结合前显著下调。这些结果表明细胞对PDGF反应的调节发生了变化，并可能表明受损血管壁的修复延迟，导致烟雾病患者动脉内膜增殖率较慢，但略长一些。