Fibrinogen, fibrin, and FDP induce C-reactive protein generation in rat vascular smooth muscle cells: Pro-inflammatory effect on atherosclerosis
Fibrinogen, fibrin, and FDP induce C-reactive protein generation in rat vascular smooth muscle cells: Pro-inflammatory effect on atherosclerosis
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DOI：
10.1016/j.bbrc.2009.10.082
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发表时间：
2009-12-18
影响因子：
3.1
通讯作者：
Lu, Peipei
中科院分区：
文献类型：
--
作者：
Guo, Fang;Liu, Juntian;Lu, Peipei
动脉粥样硬化是血管中的一种慢性炎症性疾病。C反应蛋白(CRP)作为一种炎性细胞因子，通过多种生物活性参与动脉粥样硬化的发病过程。高纤维蛋白原血症与动脉粥样硬化的形成和发展密切相关，已被广泛接受。但是，目前尚不清楚纤维蛋白原是否对血管平滑肌细胞(VSMCs)有促炎作用。本研究的目的是观察纤维蛋白原、纤维蛋白和纤维蛋白降解产物(FDP)对血管平滑肌细胞产生C反应蛋白的影响。用逆转录聚合酶链式反应检测CRPmRNA的表达。采用酶联免疫吸附试验检测VSMCs培养上清液中的CRP水平。免疫细胞化学方法检测VSMC中CRP的表达。结果表明，纤维蛋白原、纤维蛋白和FDP均能诱导VSMC产生CRP，并呈时间和浓度依赖性。其效力为FDP>；纤维蛋白原，这似乎意味着它们的促炎活性随着这三种蛋白质分子量的增加而降低。这一发现为纤维蛋白原和FDP的致动脉粥样硬化作用提供了新的机制，并强调了治疗高纤维蛋白原血症在动脉粥样硬化中的重要性。(C)2009 Elsevier Inc.保留所有权利。
Atherosclerosis is a chronic inflammatory disease in the vessel. As an inflammatory cytokine, C-reactive protein (CRP) participates in the pathogenesis of atherosclerosis through multiple bioactivities. It has been widely accepted that hyperfibrinogenemia is associated with the formation and progression of atherosclerosis. But, it is unknown whether fibrinogen exerts a pro-inflammatory effect on vascular smooth muscle cells (VSMCs). The purpose of the present Study was to observe the effect of fibrinogen, fibrin, and fibrin degradation products (FDP) on CRP generation in VSMCs. CRP mRNA expression was identified with the reverse transcription polymerase chain reaction. CRP level in the supernatant of VSMCs was measured with the enzyme-linked immunosorbent assay. CRP expression in VSMCs was examined with the immunocytochemical method. The results showed that fibrinogen, fibrin, and FDP all induced CRP production in VSMCs both in mRNA level and in protein level in a time- and concentration-dependent manner. The potency is FDP > fibrin >fibrinogen, which seems to mean that their pro-inflammatory activity decreases with increase of molecular weight of these three proteins. The finding provides a new mechanism for atherogenic effect of fibrin(ogen) and FDP, and emphasizes the importance of therapy of hyperfibrinogenemia in atherosclerosis. (C) 2009 Elsevier Inc. All rights reserved.