[动脉粥样硬化脂蛋白(a)作为肾小球疾病的进展因子:在培养的大鼠系膜细胞中的研究]。

Immunitat und Infektion Pub Date : 1995-04-01
S Greiber, M Gutenkunst, C Wanner
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引用次数: 0

摘要

脂蛋白异常是动脉粥样硬化性疾病的危险因素,被认为加速肾小球损伤。肾病综合征患者血清Lp(a)水平升高,病变肾小球中发现Lp(a)沉积。由于系膜细胞增多是多种肾小球疾病的一个突出特征,我们研究了Lp(a)对培养大鼠系膜细胞增殖的影响。在Lp(a)存在下培养的细胞中,DNA合成受到刺激,c-fos和c-myc的mRNA水平也受到刺激,这两个“早期基因”作为转录因子。与对照细胞相比,Lp(a)也加速了细胞生长42 +/- 6%。当细胞与Lp(a)在氧自由基清除剂CAT和SOD存在下孵育时,增加的DNA合成部分钝化。我们得出结论,Lp(a)异常可能导致肾脏疾病的肾小球损伤。Lp(a)改变系膜细胞增殖速率的机制与活性氧的形成有关。
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[Atherogenic lipoprotein(a) as a progression factor in glomerular diseases: studies in cultured rat mesangial cells].

Lipoprotein abnormalities are a risk factor for atherosclerotic disease and considered to accelerate glomerular injury in kidney disease. Serum levels of Lp(a) are elevated in patients with nephrotic syndrome and Lp(a) deposits are found in diseased glomeruli. Since mesangial hypercellularity is a prominent feature in a variety of glomerular diseases, we studied the effects of Lp(a) on proliferation of cultured rat mesangial cells. DNA synthesis was stimulated in cells incubated in the presence of Lp(a) as were the mRNA levels for c-fos and c-myc, two "early genes" that serve as transcription factors. Lp(a) also accelerated cell growth by 42 +/- 6% compared to control cells. Increased DNA synthesis was partially blunted, when cells were incubated with Lp(a) in the presence of oxygen radical scavengers CAT and SOD. We conclude that Lp(a) abnormalities are likely to contribute to glomerular injury in kidney disease. The mechanism by which Lp(a) alters the proliferation rate of mesangial cells involves the formation of reactive oxygen species.

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