mRNA expression of complement components and regulators in rat arterial smooth muscle cells

被引:18
作者
Li, WX
Tada, T [1 ]
Miwa, T
Okada, N
Ito, J
Okada, H
Tateyama, H
Eimoto, T
机构
[1] Nagoya City Univ, Sch Med, Dept Pathol, Mizuho Ku, Aichi 4678601, Japan
[2] Nagoya City Univ, Sch Med, Dept Mol Biol, Aichi 4678601, Japan
[3] Nagoya City Univ, Sch Med, Dept Biochem, Aichi 4678601, Japan
关键词
artery; smooth muscle cell; complement; complement regulator; cytokine;
D O I
10.1111/j.1348-0421.1999.tb02445.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The presence of C5b-9 complexes, some complement regulators, and abundant cytokines in atherosclerotic lesions has been reported. However, it is unclear whether these complement-associated proteins are produced by vascular smooth muscle cells (SMCs) and how they are influenced by the cytokines, In the present study, we demonstrated, by the reverse transcription-polymerase chain reaction method, the mRNA expression of complement components (C3, C4, and C5) and membrane regulators (decay-accelerating factor, membrane cofactor protein, Crry, and CD59) in cultured SMCs derived from the rat carotid artery. The expression of C9 mRNA was also induced upon stimulation by interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha) and/or lipopolysaccharide (LPS), Northern blot analysis showed that the mRNA expression of C3, C4, DAF and Crry was up-regulated, but that of CD59 was down-regulated by IFN-gamma, TNF-alpha and/or LPS alone or by synergy The increase of C3 mRNA by TNF-or or LPS and that of C4 mRNA by IFN-gamma was induced in a dose-dependent manner. The results indicate that the arterial SMCs of rat have the ability to produce complement components and regulators, which is affected by cytokines and/or LPS, Since atherosclerosis is characterized by the intimal proliferation of SMCs, the complement system including its regulators may be involved in the pathogenesis of the disease.
引用
收藏
页码:585 / 593
页数:9
相关论文
共 65 条
[1]   Tumour necrosis factor-alpha up-regulates decay-accelerating factor gene expression in human intestinal epithelial cells [J].
Andoh, A ;
Fujiyama, Y ;
Sumiyoshi, K ;
Sakumoto, H ;
Okabe, H ;
Bamba, T .
IMMUNOLOGY, 1997, 90 (03) :358-363
[2]   THE COMPLETE SEQUENCE OF A FULL LENGTH CDNA FOR HUMAN-LIVER GLYCERALDEHYDE-3-PHOSPHATE DEHYDROGENASE - EVIDENCE FOR MULTIPLE MESSENGER-RNA SPECIES [J].
ARCARI, P ;
MARTINELLI, R ;
SALVATORE, F .
NUCLEIC ACIDS RESEARCH, 1984, 12 (23) :9179-9189
[3]   DAMAGE TO MAMMALIAN-CELLS BY PROTEINS THAT FORM TRANSMEMBRANE PORES [J].
BHAKDI, S ;
TRANUMJENSEN, J .
REVIEWS OF PHYSIOLOGY BIOCHEMISTRY AND PHARMACOLOGY, 1987, 107 :147-223
[4]   The cell biology of atherosclerosis - new developments [J].
Campbell, JH ;
Campbell, GR .
AUSTRALIAN AND NEW ZEALAND JOURNAL OF MEDICINE, 1997, 27 (04) :497-500
[5]   DNAzol(R): A reagent for the rapid isolation of genomic DNA [J].
Chomczynski, P ;
Mackey, K ;
Drews, R ;
Wilfinger, W .
BIOTECHNIQUES, 1997, 22 (03) :550-553
[6]   IDENTIFICATION OF AN ADDITIONAL CLASS OF C3-BINDING MEMBRANE-PROTEINS OF HUMAN PERIPHERAL-BLOOD LEUKOCYTES AND CELL-LINES [J].
COLE, JL ;
HOUSLEY, GA ;
DYKMAN, TR ;
MACDERMOTT, RP ;
ATKINSON, JP .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1985, 82 (03) :859-863
[7]   CD59, AN LY-6-LIKE PROTEIN EXPRESSED IN HUMAN LYMPHOID-CELLS, REGULATES THE ACTION OF THE COMPLEMENT MEMBRANE ATTACK COMPLEX ON HOMOLOGOUS CELLS [J].
DAVIES, A ;
SIMMONS, DL ;
HALE, G ;
HARRISON, RA ;
TIGHE, H ;
LACHMANN, PJ ;
WALDMANN, H .
JOURNAL OF EXPERIMENTAL MEDICINE, 1989, 170 (03) :637-654
[8]  
GASQUE P, 1995, J IMMUNOL, V154, P4726
[9]   FUNCTIONAL ANGIOTENSIN-II RECEPTORS IN CULTURED VASCULAR SMOOTH-MUSCLE CELLS [J].
GUNTHER, S ;
ALEXANDER, RW ;
ATKINSON, WJ ;
GIMBRONE, MA .
JOURNAL OF CELL BIOLOGY, 1982, 92 (02) :289-298
[10]  
HARADA R, 1990, J IMMUNOL, V144, P1823