Fibrinogen, fibrin, and FDP induce C-reactive protein generation in rat vascular smooth muscle cells: Pro-inflammatory effect on atherosclerosis

被引:20
作者
Guo, Fang [1 ]
Liu, Juntian [1 ]
Wang, Chenjing
Liu, Na [1 ]
Lu, Peipei [1 ]
机构
[1] Xi An Jiao Tong Univ, Dept Pharmacol, Sch Med, Xian 710061, Peoples R China
关键词
Fibrinogen; Fibrin; Fibrin degradation products; C-reactive protein; Vascular smooth muscle cells; Atherosclerosis; HUMAN ENDOTHELIAL-CELLS; CARDIOVASCULAR-DISEASE; INTERLEUKIN-6; ATHEROGENESIS; EXPRESSION;
D O I
10.1016/j.bbrc.2009.10.082
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:942 / 946
页数:5
相关论文
共 26 条
[1]   Interrelationships among circulating interleukin-6, C-reactive protein, and traditional cardiovascular risk factors in women [J].
Bermudez, EA ;
Rifai, N ;
Buring, J ;
Manson, JE ;
Ridker, PA .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2002, 22 (10) :1668-1673
[2]   Inflammatory cytokines stimulated C-reactive protein production by human coronary artery smooth muscle cells [J].
Calabró, P ;
Willerson, JT ;
Yeh, ETH .
CIRCULATION, 2003, 108 (16) :1930-1932
[3]   Inflammation, thrombosis and atherosclerosis: results of the Glostrup study [J].
De Maat, MPM ;
Bladbjerg, EM ;
Drivsholm, T ;
Borch-Johnsen, K ;
Moller, L ;
Jespersen, J .
JOURNAL OF THROMBOSIS AND HAEMOSTASIS, 2003, 1 (05) :950-957
[4]   Inflammation, atherosclerotic burden and cardiovascular prognosis [J].
Espinola-Klein, Christine ;
Rupprecht, Hans J. ;
Bickel, Christoph ;
Lackner, Karl ;
Schnabel, Renate ;
Munzel, Thomas ;
Blankenberg, Stefan .
ATHEROSCLEROSIS, 2007, 195 (02) :E126-E134
[5]   Elevated fibrinogen levels and subsequent subclinical atherosclerosis: The CARDIA Study [J].
Green, David ;
Foiles, Nancy ;
Chan, Cheeling ;
Schreinere, Pamela J. ;
Liu, Kiang .
ATHEROSCLEROSIS, 2009, 202 (02) :623-631
[6]  
Greiling D, 1997, J CELL SCI, V110, P861
[7]   ABNORMALITIES IN GROWTH-CHARACTERISTICS OF AORTIC SMOOTH-MUSCLE CELLS IN SPONTANEOUSLY HYPERTENSIVE RATS [J].
HADRAVA, V ;
TREMBLAY, J ;
HAMET, P .
HYPERTENSION, 1989, 13 (06) :589-597
[8]   Mechanisms of disease - Inflammation, atherosclerosis, and coronary artery disease [J].
Hansson, GK .
NEW ENGLAND JOURNAL OF MEDICINE, 2005, 352 (16) :1685-1695
[9]   Fibrinogen [J].
Herrick, S ;
Blanc-Brude, O ;
Gray, A ;
Laurent, G .
INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY, 1999, 31 (07) :741-746
[10]   Vasoactive effects of fibrinogen on saphenous vein [J].
Hicks, RCJ ;
Golledge, J ;
MirHasseine, R ;
Powell, JT .
NATURE, 1996, 379 (6568) :818-820