期刊
EXPERIMENTAL AND MOLECULAR MEDICINE
卷 39, 期 1, 页码 97-105出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/emm.2007.11
关键词
asthma; bronchial hype rreactivity; epithelial cells; matrix metalloproteinase 9; NF-kappa B; protein kinase C-alpha
Expression of matrix metalloproteinase-9 (MMP-9) is associated with airway remodeling and tissue injury in asthma. However, little is known about how MMP-9 is up-regulated in airway epithelial cells. In this study, we show that phorbol myristate acetate (PMA) induces MMP-9 expression via a protein kinase C alpha (PKC alpha)-dependent signaling cascade in BEAS-2B human lung epithelial cells. Pretreatment with either GF109203X, a general PKC inhibitor, or Go6976, a PKC alpha/beta isozyme inhibitor, inhibited PMA-induced activation of the MMP-9 promoter, as did transient transfection with PKC alpha antisense oligonuclotides. PMA activated NF-kappa B by phosphorylating I kappa B in these cells and this was also inhibited by GF109203X and Go6976, suggesting that PKC alpha acts as an upstream regulator of NF-kappa B in PMA-induced MMP-9 induction. Our results indicate that a PKC alpha-NF-kappa B-dependent cascade is involved in the signaling leading to PMA-induced MMP-9 expression in the lung epithelium.
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