Journal of dermatological science · 2006
Cytokine modulation of retinoic acid-inducible gene-I (RIG-I) expression in human epidermal keratinocytes.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Kitamura Hideo, Matsuzaki Yasushi, Kimura Kazuyuki, Nakano Hajime, Imaizumi Tadaatsu, Satoh Kei, Hanada Katsumi
Аннотация
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: Our results suggest that RIG-I might operate not only as a RNA helicase but also as a mediator of the cytokine network in the inflammatory skin diseases, such as psoriasis vulgaris.
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: Our results suggest that RIG-I might operate not only as a RNA helicase but also as a mediator of the cytokine network in the inflammatory skin diseases, such as psoriasis vulgaris.