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首页> 外文期刊>Journal of Cellular Physiology >Low density lipoprotein receptor-related protein 1 modulates the proliferation and migration of human hepatic stellate cells
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Low density lipoprotein receptor-related protein 1 modulates the proliferation and migration of human hepatic stellate cells

机译：低密度脂蛋白受体相关蛋白1调节的增殖和迁移人肝星状细胞

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Human hepatic stellate cells (HHSCs) proliferation and migration play a key role in the pathogenesis of liver inflammation and fibrogenesis. Low density lipoprotein receptor-related protein (LRP1) is an endocytic receptor involved in intracellular signal transduction. The aim of this work was to analyse the role of low density lipoprotein receptor-related protein (LRP1) in HHSCs proliferation and migration and the mechanisms involved. Human LRP1 deficient-HHSCs were generated by nucleofecting the line HHSCs with siRNA anti-LRP1. HHSCs DNA synthesis was measured by [ 3H]-thymidine incorporation and cell cycle progression by flow cytometry after annexin V and iodure propidium staining. Cell migration was assessed using a wound repair model system. LRP1 expression and extracellular matrix-regulated kinase (ERK1,2) phosphorylation were analysed by Western blot analysis. Transforming growth factor-β (TGF-β) extracellular levels were analysed by ELISA. siRNA-antiLRP1 treatment almost completely inhibited LRP1 mRNA and protein expression. LRP1 deficient HHSCs showed higher proliferative response (172±19 vs. 93±8 [ 3H]-thymidine incorporation; 78.68% vs. 82.69% in G0/G1, 21.32% vs. 17.30% in G2/S) and higher migration rates than control HHSCs. LRP1 deficient cells showed higher levels of phosphorylated ERK1,2. TGF-β extracellular levels were threefold higher in LRP1-deficient than in control HHSCs cells. These results demonstrate that LRP1 regulates HHSCs proliferation and migration through modulation of ERK1,2 phosphorylation and TGF-β extracellular levels. These results suggest that HHSCs-LRP1 may play a key role in the modulation of factors determining hepatic fibrosis. J. Cell. Physiol. 227: 3528-3533, 2012.
机译：人肝星状细胞(HHSCs)扩散发病机制和迁移起着关键的作用肝脏的炎症和纤维发生。密度脂蛋白受体相关蛋白(LRP1恰巧)是一种内吞作用的受体参与细胞内信号转导。这项工作是分析低密度的作用脂蛋白受体相关蛋白(LRP1恰巧)HHSCs增殖和迁移机制。是由nucleofecting HHSCs行吗siRNA anti-LRP1。衡量[3 h]胸腺嘧啶核苷掺入细胞周期进展后,流式细胞术膜联蛋白V和iodure propidium染色。迁移是由伤口修复模型系统。matrix-regulated激酶磷酸化(ERK1 2)分析了通过免疫印迹分析。转化生长因子-β(TGF -β)细胞外被ELISA分析水平。siRNA-antiLRP1治疗几乎完全抑制LRP1恰巧mRNA和蛋白表达。缺乏HHSCs显示更高的增殖响应(172±19和93±8 [3 h]胸苷合并;在G2 / S比17.30%)和高迁移率HHSCs比控制。更高水平的磷酸化ERK1 2。细胞外水平高出三倍比控制LRP1-deficient HHSCs细胞。结果表明,LRP1恰巧调节HHSCs通过调制的增殖和迁移ERK1 2磷酸化和TGF -β细胞外的水平。调制中发挥关键作用的因素确定肝纤维化。227: 3528-3533, 2012.

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