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首页> 外文期刊>Life sciences >Low density lipoproteins transactivate EGF receptor: role in mesangial cell proliferation.
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Low density lipoproteins transactivate EGF receptor: role in mesangial cell proliferation.

机译：低密度脂蛋白激活EGF受体：在肾小球膜细胞增殖中的作用。

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摘要

Hyperlipidemia and the glomerular accumulation of atherogenic lipoproteins (low density lipoprotein, LDL; and its oxidatively-modified variants, ox-LDL) are commonly associated with the development of glomerular mesangial proliferative diseases. However, cellular signaling mechanisms by which atherogenic lipoproteins stimulate mesangial cell proliferation are poorly defined. In this study, we examined the effect of atherogenic lipoproteins on the activation of mesangial cell epidermal growth factor (EGF) receptor, mitogen activated protein kinase (MAP kinase), Ras, and mesangial cell proliferation. Stimulation of mesangial cells with LDL, and with greater activity, ox-LDL, markedly induced the transactivation of EGF receptor within 5 min of stimulation; the effect persisted up to at least 60 min LDL, and with a greater degree, ox-LDL, increased the activation of Ras, MAP kinase, and mesangial cell proliferation. Inhibition of EGF receptor kinase activity and/or MAP kinase activation blocked both LDL- and ox-LDL-induced mesangial cell proliferation. We suggest that the accumulation of LDL and more potently its oxidized forms within the glomerulus, through the transactivation of EGF receptor, stimulate down-stream Ras-MAP kinase signaling cascade leading to mesangial cell proliferation. Regulation of glomerular accumulation of atherogenic lipoproteins and/or EGF receptor signaling may provide protective environment against mesangial hypercellularity seen in glomerular diseases.
机译：高脂血症和动脉粥样硬化脂蛋白（低密度脂蛋白，LDL;及其氧化修饰的变体，ox-LDL）的肾小球积聚通常与肾小球系膜增生性疾病的发展有关。但是，动脉粥样硬化脂蛋白刺激肾小球膜细胞增殖的细胞信号传导机制尚不明确。在这项研究中，我们检查了动脉粥样硬化性脂蛋白对肾小球系膜细胞表皮生长因子（EGF）受体，促分裂原活化蛋白激酶（MAP激酶），Ras和肾小球系膜细胞增殖的影响。用LDL和活性更高的ox-LDL刺激肾小球系膜细胞在刺激后5分钟内能明显诱导EGF受体的反式激活。该作用持续至少60分钟LDL，并且ox-LDL在更大程度上增强了Ras，MAP激酶和系膜细胞增殖的激活。 EGF受体激酶活性和/或MAP激酶激活的抑制阻止LDL和ox LDL诱导的系膜细胞增殖。我们建议通过EGF受体的反式激活，肾小球内LDL的积累以及更有效地其氧化形式的积累，刺激下游Ras-MAP激酶信号传导级联反应，导致肾小球膜细胞增殖。调节动脉粥样硬化脂蛋白的肾小球积聚和/或EGF受体信号转导可提供针对肾小球疾病中所见的肾小球膜高细胞性的保护环境。

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