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KMID : 0361020150580090615
Korean Journal of Otolaryngology - Head and Neck Surgery
2015 Volume.58 No. 9 p.615 ~ p.621
Effect of Polyinosinic-Polycytidylic Acid on MUC5B Expression in Human Airway Epithelial Cells
ÃÖ¿äÇÑ:Choi Yo-Han
¹èâÈÆ:Bae Chang-Hoon/±èÇü±Ù:Kim Hyeong-Geun/¼­º¸Çö:Seo Bo-Hyeon/ÃÖÀ±¼®:Choi Yoon-Seok/¼Û½Ã¿¬:Song Si-Youn/±è¿ë´ë:Kim Yong-Dae
Abstract
Background and Objectives: Polyinosinic-polycytidylic acid (Poly I:C) is structurally similar to double-stranded RNA, and is known to induce various inflammatory mediators and to cause inflammatory reactions in airway epithelial cells. However, the effect of Poly I:C on secretion of mucins in human airway epithelial cells has been very rarely reported. In this study, the effect and brief signaling pathway of Poly I:C on the expression of mucin genes were investigated in human airway epithelial cells.

Materials and Method: In mucin-producing human NCI-H292 airway epithelial cells and the primary cultures of normal human nasal epithelial cells, the effect and signaling pathway of Poly I:C on expression of mucin genes were investigated using reverse transcriptase-polymerase chain reaction, real-time PCR, enzyme immunoassay, and immunoblot analysis with specific inhibitors and small interfering RNA (siRNA) for mitogen-activated protein kinase (MAPK).

Results: Poly I:C induced the MUC5B expression, and activated the phosphorylation of ERK1/2 and p38 MAPK. U0126 (ERK1/2 MAPK inhibitor) and SB203580 (p38 MAPK inhibitor) inhibited the Poly I:C-induced MUC5B expression. In addition, the knockdown of ERK2 and p38 MAPK by siRNA significantly blocked the Poly I:C-induced MUC5B mRNA expression.

Conclusion: Poly I:C induces the MUC5B expression via ERK2 and p38 MAPK signaling pathways in human airway epithelial cells. Therefore, Poly I:C may play a role in the regulation of mucus hypersecretion through MAPK signaling pathways in the human airway epithelial cells.
KEYWORD
Human airway epithelial cells, Mitogen-activated protein kinase, MUC5B, Polyinosinic-polycytidylic acid
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