Possible involvements of nuclear factor-κB and activator protein-1 in the tumor necrosis factor-α-induced upregulation of matrix metalloproteinase-12 in human alveolar epithelial A549 cell line
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- Yu Yingyan
- Department of Pharmacology, School of Pharmacy, Hoshi University, Japan
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- Chiba Yoshihiko
- Department of Pharmacology, School of Pharmacy, Hoshi University, Japan
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- Sakai Hiroyasu
- Department of Pharmacology, School of Pharmacy, Hoshi University, Japan
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- Misawa Miwa
- Department of Pharmacology, School of Pharmacy, Hoshi University, Japan
書誌事項
- タイトル別名
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- Possible Involvements of Nuclear Factor-.KAPPA.B and Activator Protein-1 in the Tumor Necrosis Factor-.ALPHA.-Induced Upregulation of Matrix Metalloproteinase-12 in Human Alveolar Epithelial A549 Cell Line
- Possible involvements of nuclear factor カッパ B and activator protein 1 in the tumor necrosis factor a induced upregulation of matrix metalloproteinase 12 in human alveolar epithelial A549 cell line
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Matrix metalloproteinase-12 (MMP-12) has been suggested to play an important role in airway inflammatory diseases. Tumor necrosis factor-α (TNF-α) is known to cause an upregulation of MMP-12 via an activation of activator protein-1 (AP-1) in monocytes. In the present study, we investigated the effect of TNF-α on the expressions of MMP-12 in airway epithelial cells, one of the sources of MMP-12 in the airway, and its underlying mechanism. MMP-12 mRNA and protein expressions induced by TNF-α in the absence or presence of BMS-345541 (a selective IκB kinase inhibitor) or SP600125 [a selective c-Jun N-terminal kinase (JNK) inhibitor] were measured by quantitative real-time PCR and Western blotting, respectively. Furthermore, siRNAs for p65 and JNK2 were used to confirm the involvements of nuclear factor-κB (NF-κB) and AP-1 in the MMP-12 mRNA expression induced by TNF-α in A549 cells. Both MMP-12 mRNA and protein were upregulated by the treatment with TNF-α in time- and concentration-dependent manners. Both BMS-345541 and SP600125 inhibited the upregulation of MMP-12 induced by TNF-α. Furthermore, both the depletion of p65 and JNK2 by siRNAs significantly attenuated the upregulation of MMP-12 induced by TNF-α. These findings suggest that both NF-κB and JNK / AP-1 pathways are important for the MMP-12 upregulation induced by TNF-α in A549 cells.
収録刊行物
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- Journal of Pharmacological Sciences
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Journal of Pharmacological Sciences 112 (1), 83-88, 2010
公益社団法人 日本薬理学会
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詳細情報 詳細情報について
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- CRID
- 1390001205181302016
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- NII論文ID
- 130000148446
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- NII書誌ID
- AA11806667
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- ISSN
- 13478648
- 13478613
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- NDL書誌ID
- 10524852
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
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- 使用不可