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mRNA Expression of Complement Components and Regulators in Rat Arterial Smooth Muscle Cells
Author(s) -
Li Wenxin,
Tada Toyohiro,
Miwa Takashi,
Okada Noriko,
Ito Jinichi,
Okada Hidechika,
Tateyama Hisashi,
Eimoto Tadaaki
Publication year - 1999
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/j.1348-0421.1999.tb02445.x
Subject(s) - cd59 , biology , decay accelerating factor , lipopolysaccharide , complement membrane attack complex , tumor necrosis factor alpha , messenger rna , vascular smooth muscle , northern blot , complement system , microbiology and biotechnology , immunology , endocrinology , antibody , gene , biochemistry , smooth muscle
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‐γ), tumor necrosis factor‐alpha (TNF‐α) 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‐7, TNF‐α and/or LPS alone or by synergy. The increase of C3 mRNA by TNF‐α or LPS and that of C4 mRNA by IFN‐γ 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.