Abstract | BACKGROUND: OBJECTIVES: METHODS: Cell proliferation assay, immunostaining, immunoblotting, cell enzyme-linked immunosorbent assay and reverse transcriptase-polymerase chain reaction (RT-PCR) were performed to examine the effects of MTX on HUVEC. RESULTS: MTX inhibited the proliferation of HUVEC at 10-7 mol L-1 and 10-6 mol L-1 without showing cytotoxic effects. It also inhibited TNF-alpha-induced ICAM-1 and VCAM-1 expression by HUVEC at 10-6 mol L-1. The inhibitory effect of MTX was more pronounced on ICAM-1 expression than on VCAM-1 expression. RT-PCR analysis revealed that TNF-alpha-induced ICAM-1 gene expression was strongly downregulated by MTX. CONCLUSIONS: Low-dose MTX may act on psoriasis by suppressing the TNF-alpha-induced expression of ICAM-1 and VCAM-1 by vascular endothelial cells. Inhibition of neovascularization may be another mechanism of action of MTX.
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Authors | E Yamasaki, Y Soma, Y Kawa, M Mizoguchi |
Journal | The British journal of dermatology
(Br J Dermatol)
Vol. 149
Issue 1
Pg. 30-8
(Jul 2003)
ISSN: 0007-0963 [Print] England |
PMID | 12890192
(Publication Type: Journal Article)
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Chemical References |
- Immunosuppressive Agents
- Tumor Necrosis Factor-alpha
- Vascular Cell Adhesion Molecule-1
- Intercellular Adhesion Molecule-1
- Methotrexate
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Topics |
- Blotting, Western
- Cell Division
(drug effects)
- Cells, Cultured
- Dose-Response Relationship, Drug
- Down-Regulation
(drug effects)
- Endothelium, Vascular
(cytology, drug effects, metabolism)
- Humans
- Immunosuppressive Agents
(pharmacology)
- Intercellular Adhesion Molecule-1
(genetics, metabolism)
- Methotrexate
(pharmacology)
- Reverse Transcriptase Polymerase Chain Reaction
- Tumor Necrosis Factor-alpha
(pharmacology)
- Vascular Cell Adhesion Molecule-1
(metabolism)
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