2010年
Expression of Phosphatidylserine-Specific Phospholipase A(1) mRNA in Human THP-1-Derived Macrophages
CELL TRANSPLANTATION
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- 巻
- 19
- 号
- 6-7
- 開始ページ
- 759
- 終了ページ
- 764
- 記述言語
- 英語
- 掲載種別
- DOI
- 10.3727/096368910X508861
- 出版者・発行元
- COGNIZANT COMMUNICATION CORP
The expression of phosphatidylserine-specific phospholipase A(1) (PS-PLA(1)) is most upregulated in the genes of peripheral blood cells from chronic rejection model rats bearing long-term surviving cardiac allografts. The expression profile of PS-PLA(1) in peripheral blood cells responsible for the immune response may indicate a possible biological marker for rejection episodes. In this study, PS-PLA(1) mRNA expression was examined in human THP-1-derived macrophages. The effects of several immunosuppressive agents on this expression were also examined in in vitro experiments. A real-time RT-PCR analysis revealed that PS-PLA(1) mRNA expression was found in human THP-1-derived macrophages. This expression was enhanced in the cells stimulated with lipopolysaccharide (LPS), a toll-like receptor (TLR) 4 ligand. Other TLR ligands (TLR2, 3, 5, 7, and 9) did not show a significant induction of PS-PLA(1) mRNA. The time course of the mRNA expression profiles was different between PS-PLA(1) and tumor necrosis factor-alpha (TNF-alpha), which showed a maximal expression at 12 and I h after LPS stimulation, respectively. Among the observed immunosuppressive agents, corticosteroids, prednisolone, 6 alpha-methylprednisolone, dexamethasone, and beclomethasone inhibited PS-PLA(1) expression with half-maximal inhibitory concentrations less than 3.0 nM, while methotrexate, cyclosporine A, tacrolimus, 6-mercaptopurine, and mycophenoic acid showed either a weak or moderate inhibition. These results suggest that the expression of PS-PLA(1) mRNA in THP-1-derived macrophages is activated via TLR4 and it is inhibited by corticosteroids, which are used at high dosages to suppress chronic allograft rejection.
- リンク情報
- ID情報
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- DOI : 10.3727/096368910X508861
- ISSN : 0963-6897
- Web of Science ID : WOS:000282860500014