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氧化型低密度脂蛋白通过 IGF2 通路在上皮细胞 THP-1 中上调 CRP 表达。

Ox-LDL upregulates CRP expression through the IGF2 pathway in THP-1 macrophages.

机构信息

Laboratory Medicine Center, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, 510515, China.

出版信息

Inflammation. 2015 Apr;38(2):576-83. doi: 10.1007/s10753-014-9964-4.

Abstract

C-reactive protein (CRP) is an acute-phase reactant protein that not only plays a predictive role in determining atherogenesis risk but also represents an active participant in atherogenesis onset and progression. Moreover, an increasing number of studies have reported that oxidized low-density lipoprotein (Ox-LDL) plays a significant role in the initiation and progression of atherosclerosis. However, the effect and underlying mechanism of Ox-LDL on CRP expression remains unclear. THP-1 macrophages were treated with 0, 25, 50, or 100 μg/mL of Ox-LDL for 48 h, or 50 μg/mL of Ox-LDL for 0, 12, 24, and 48 h, respectively. Messenger RNA (mRNA) and protein levels were measured by real-time quantitative PCR and Western blot analysis, respectively. We found that Ox-LDL markedly increased insulin-like growth factor 2 (IGF2) and CRP mRNA and protein levels in a dose- and time-dependent manner in THP-1 macrophages. Treatment with Ox-LDL increased CRP protein expression, and this effect was completely abolished by siRNA-mediated silencing of IGF2 in THP-1 macrophages. Moreover, treatment with pcDNA3.1-IGF2 significantly enhanced CRP protein expression in Ox-LDL-stimulated THP-1 macrophages. CRP expression is upregulated by Ox-LDL through the IGF2 pathway in THP-1 macrophages.

摘要

C-反应蛋白(CRP)是一种急性期反应物蛋白,不仅在预测动脉粥样硬化形成风险方面发挥作用,而且还是动脉粥样硬化发生和进展的积极参与者。此外,越来越多的研究报告指出,氧化型低密度脂蛋白(Ox-LDL)在动脉粥样硬化的发生和进展中起着重要作用。然而,Ox-LDL 对 CRP 表达的影响及其潜在机制尚不清楚。用 0、25、50 或 100μg/ml 的 Ox-LDL 分别处理 THP-1 巨噬细胞 48 小时,或用 50μg/ml 的 Ox-LDL 分别处理 THP-1 巨噬细胞 0、12、24 和 48 小时,然后分别通过实时定量 PCR 和 Western blot 分析测量信使 RNA(mRNA)和蛋白质水平。我们发现 Ox-LDL 可明显增加 THP-1 巨噬细胞中胰岛素样生长因子 2(IGF2)和 CRP 的 mRNA 和蛋白水平,呈剂量和时间依赖性。Ox-LDL 处理增加了 CRP 蛋白的表达,而在 THP-1 巨噬细胞中用 IGF2 的 siRNA 介导沉默则完全消除了这种作用。此外,pcDNA3.1-IGF2 的处理显著增强了 Ox-LDL 刺激的 THP-1 巨噬细胞中 CRP 蛋白的表达。Ox-LDL 通过 THP-1 巨噬细胞中的 IGF2 途径上调 CRP 表达。

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