Abstract | BACKGROUND:
Retinoic acid-inducible gene-I (RIG-I) is a member of the DExH/D box family proteins and designated as a putative RNA helicase, which plays various roles in gene expression and cellular functions in response to a variety of RNA viruses. OBJECTIVE: The present study was designed to investigate the effects of interferon (IFN)-gamma and tumor necrosis factor ( TNF)-alpha on RIG-I expression in human keratinocytes, and the expression of RIG-I in skin lesions of psoriasis vulgaris, in which IFN-gamma and TNF-alpha are considered to be involved in its pathogenesis. METHODS: The mRNA and protein expression of RIG-I was analyzed by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting. Immunohistochemical staining of RIG-I was examined on psoriatic skin section. RESULTS: The levels of RIG-I mRNA and protein were upregulated in HaCaT keratinocytes in the presence of IFN-gamma or TNF-alpha. Immunohistochemically, RIG-I was detected in the cytoplasm of the spinous and basal layers of psoriatic skin. CONCLUSION:
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Authors | Hideo Kitamura, Yasushi Matsuzaki, Kazuyuki Kimura, Hajime Nakano, Tadaatsu Imaizumi, Kei Satoh, Katsumi Hanada |
Journal | Journal of dermatological science
(J Dermatol Sci)
Vol. 45
Issue 2
Pg. 127-34
(Feb 2007)
ISSN: 0923-1811 [Print] Netherlands |
PMID | 17182220
(Publication Type: Journal Article)
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Chemical References |
- RNA, Messenger
- Receptors, Immunologic
- Tumor Necrosis Factor-alpha
- Interferon-gamma
- RIGI protein, human
- DEAD Box Protein 58
- DEAD-box RNA Helicases
- RNA Helicases
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Topics |
- Adult
- Aged
- Biopsy
- Cell Line, Transformed
- Cytoplasm
(metabolism)
- DEAD Box Protein 58
- DEAD-box RNA Helicases
(genetics, metabolism)
- Epidermal Cells
- Gene Expression
(drug effects)
- Humans
- Interferon-gamma
(metabolism, pharmacology)
- Keratinocytes
(cytology, physiology)
- Middle Aged
- Psoriasis
(pathology, physiopathology)
- RNA Helicases
(genetics, metabolism)
- RNA, Messenger
(metabolism)
- Receptors, Immunologic
- Tumor Necrosis Factor-alpha
(metabolism, pharmacology)
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