호흡기 상피세포에서 PKC-MEK/ERK 활성화를 통한 IL-1β에 의한 Cyclooxygenase-2 발현

김용대; 송시연; 백석환; 조길성; 우현재; 윤석근

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자료유형: 학술저널

저자정보: 김용대 송시연 백석환 조길성 우현재 윤석근

저널정보: 대한이비인후과학회 대한이비인후-두경부외과학회지 대한이비인후과학회지 두경부외과학 제45권 제10호

발행연도: 2002.1

수록면: 957 - 962 (6page)

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Background and Objectives：Cyclooxygenase-2 (COX-2) plays an important role in the biosynthesis of prostaglandin, which is an important inflammatory mediator in human airway inflammatory disease. We observed that interleukin-1β (IL-1β) induces COX-2 gene expression and protein production in NCI-H292 cells in the previous experiment and designed this study to investigate the signal transduction pathway of the IL-1β Materials and Method：In the cultured human airway NCI-H292 epithelial cels, the IL-1β-mediated COX-2 gene and protein expresion were analyzed by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. To identify the signal transduction pathway of the IL-1β-mediated COX-2 expresion, we used specific inhibitors. Results：PD98059, MEK/ERK inhibitor sup-presed IL-1β-mediated COX-2 gene and protein expression, but SB203580, p38 inhibitor did not suppres it. Ro31-8220, PKC inhibitor attenuated IL-1β-mediated COX-2 gene and protein expresion. Ro31-8220 suppresed ERK phosphorylation, but did not inhibit phosphorylation of p38 and JNK. PKC were involved at upstream of ERK in the IL-1β-mediated COX-2 expresion. PI3K inhibitor, LY294002 and tyrosine kinase inhibitor, genistein did not suppres COX-2 expresion. Conclusion：IL-1β-in-duced COX-2 gene and protein expresion is up-regulated through activation of PKC-MEK/ERK cascade in human airway NCI-H292 epithelial cells. (Korean J Otolaryngol 2002;45:957-62)

#Interleukin-1β·Cyclooxygenase-2·Protein Kinase C·MEK/ERK.system.

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